The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.
The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.
The number of PLATELETS per unit volume in a sample of venous BLOOD.
Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. Many of these are receptors.
Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.
Laboratory examination used to monitor and evaluate platelet function in a patient's blood.
Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.
Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
The phenomenon by which dissociated cells intermixed in vitro tend to group themselves with cells of their own type.
Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.
An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).
A series of progressive, overlapping events, triggered by exposure of the PLATELETS to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug.
A CXC chemokine that is found in the alpha granules of PLATELETS. The protein has a molecular size of 7800 kDa and can occur as a monomer, a dimer or a tetramer depending upon its concentration in solution. Platelet factor 4 has a high affinity for HEPARIN and is often found complexed with GLYCOPROTEINS such as PROTEIN C.
A phospholipid derivative formed by PLATELETS; BASOPHILS; NEUTROPHILS; MONOCYTES; and MACROPHAGES. It is a potent platelet aggregating agent and inducer of systemic anaphylactic symptoms, including HYPOTENSION; THROMBOCYTOPENIA; NEUTROPENIA; and BRONCHOCONSTRICTION.
Platelet membrane glycoprotein complex essential for normal platelet adhesion and clot formation at sites of vascular injury. It is composed of three polypeptides, GPIb alpha, GPIb beta, and GPIX. Glycoprotein Ib functions as a receptor for von Willebrand factor and for thrombin. Congenital deficiency of the GPIb-IX complex results in Bernard-Soulier syndrome. The platelet glycoprotein GPV associates with GPIb-IX and is also absent in Bernard-Soulier syndrome.
The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).
Formation and development of a thrombus or blood clot in the blood vessel.
A subclass of purinergic P2Y receptors that have a preference for ADP binding and are coupled to GTP-BINDING PROTEIN ALPHA SUBUNIT, GI. The P2Y12 purinergic receptors are found in PLATELETS where they play an important role regulating PLATELET ACTIVATION.
A stable, physiologically active compound formed in vivo from the prostaglandin endoperoxides. It is important in the platelet-release reaction (release of ADP and serotonin).
The transfer of blood platelets from a donor to a recipient or reinfusion to the donor.
An antibiotic mixture of two components, A and B, obtained from Nocardia lurida (or the same substance produced by any other means). It is no longer used clinically because of its toxicity. It causes platelet agglutination and blood coagulation and is used to assay those functions in vitro.
A calcium-activated enzyme that catalyzes the hydrolysis of ATP to yield AMP and orthophosphate. It can also act on ADP and other nucleoside triphosphates and diphosphates. EC
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.
Venoms from snakes of the subfamily Crotalinae or pit vipers, found mostly in the Americas. They include the rattlesnake, cottonmouth, fer-de-lance, bushmaster, and American copperhead. Their venoms contain nontoxic proteins, cardio-, hemo-, cyto-, and neurotoxins, and many enzymes, especially phospholipases A. Many of the toxins have been characterized.
Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension (HYPERTENSION, PULMONARY).
Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase.
Disorders caused by abnormalities in platelet count or function.
A subnormal level of BLOOD PLATELETS.
Human alloantigens expressed only on platelets, specifically on platelet membrane glycoproteins. These platelet-specific antigens are immunogenic and can result in pathological reactions to transfusion therapy.
A stable prostaglandin endoperoxide analog which serves as a thromboxane mimetic. Its actions include mimicking the hydro-osmotic effect of VASOPRESSIN and activation of TYPE C PHOSPHOLIPASES. (From J Pharmacol Exp Ther 1983;224(1): 108-117; Biochem J 1984;222(1):103-110)
The formation of clumps of RED BLOOD CELLS under low or non-flow conditions, resulting from the attraction forces between the red blood cells. The cells adhere to each other in rouleaux aggregates. Slight mechanical force, such as occurs in the circulation, is enough to disperse these aggregates. Stronger or weaker than normal aggregation may result from a variety of effects in the ERYTHROCYTE MEMBRANE or in BLOOD PLASMA. The degree of aggregation is affected by ERYTHROCYTE DEFORMABILITY, erythrocyte membrane sialylation, masking of negative surface charge by plasma proteins, etc. BLOOD VISCOSITY and the ERYTHROCYTE SEDIMENTATION RATE are affected by the amount of erythrocyte aggregation and are parameters used to measure the aggregation.
The process which spontaneously arrests the flow of BLOOD from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements (eg. ERYTHROCYTE AGGREGATION), and the process of BLOOD COAGULATION.
Synthetic compounds that are analogs of the naturally occurring prostaglandin endoperoxides and that mimic their pharmacologic and physiologic activities. They are usually more stable than the naturally occurring compounds.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.
A congenital bleeding disorder with prolonged bleeding time, absence of aggregation of platelets in response to most agents, especially ADP, and impaired or absent clot retraction. Platelet membranes are deficient in or have a defect in the glycoprotein IIb-IIIa complex (PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX).
A phospholipid from the platelet membrane that contributes to the blood clotting cascade by forming a phospholipid-protein complex (THROMBOPLASTIN) which serves as a cofactor with FACTOR VIIA to activate FACTOR X in the extrinsic pathway of BLOOD COAGULATION.
Platelet membrane glycoprotein IIb is an integrin alpha subunit that heterodimerizes with INTEGRIN BETA3 to form PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX. It is synthesized as a single polypeptide chain which is then postranslationally cleaved and processed into two disulfide-linked subunits of approximately 18 and 110 kDa in size.
Very large BONE MARROW CELLS which release mature BLOOD PLATELETS.
Univalent antigen-binding fragments composed of one entire IMMUNOGLOBULIN LIGHT CHAIN and the amino terminal end of one of the IMMUNOGLOBULIN HEAVY CHAINS from the hinge region, linked to each other by disulfide bonds. Fab contains the IMMUNOGLOBULIN VARIABLE REGIONS, which are part of the antigen-binding site, and the first IMMUNOGLOBULIN CONSTANT REGIONS. This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
Cell surface proteins that bind THROMBOXANES with high affinity and trigger intracellular changes influencing the behavior of cells. Some thromboxane receptors act via the inositol phosphate and diacylglycerol second messenger systems.
An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
A family of proteinase-activated receptors that are specific for THROMBIN. They are found primarily on PLATELETS and on ENDOTHELIAL CELLS. Activation of thrombin receptors occurs through the proteolytic action of THROMBIN, which cleaves the N-terminal peptide from the receptor to reveal a new N-terminal peptide that is a cryptic ligand for the receptor. The receptors signal through HETEROTRIMERIC GTP-BINDING PROTEINS. Small synthetic peptides that contain the unmasked N-terminal peptide sequence can also activate the receptor in the absence of proteolytic activity.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Antibodies produced by a single clone of cells.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
A subclass of eicosanoid receptors that have specificity for THROMBOXANE A2 and PROSTAGLANDIN H2.
The deformation and flow behavior of BLOOD and its elements i.e., PLASMA; ERYTHROCYTES; WHITE BLOOD CELLS; and BLOOD PLATELETS.
A subclass of purinergic P2Y receptors that have a preference for ATP and ADP. The activated P2Y1 receptor signals through the G-PROTEIN-coupled activation of PHOSPHOLIPASE C and mobilization of intracellular CALCIUM.
The rate dynamics in chemical or physical systems.
Laboratory tests for evaluating the individual's clotting mechanism.
Compounds that bind to and block the stimulation of PURINERGIC P2Y RECEPTORS. Included under this heading are antagonists for specific P2Y receptor subtypes.
Peptides composed of between two and twelve amino acids.
A dual specificity phosphatase subtype that plays a role in intracellular signal transduction by inactivating MITOGEN-ACTIVATED PROTEIN KINASES. It has specificity for EXTRACELLULAR SIGNAL-REGULATED MAP KINASES and is primarily localized to the CELL NUCLEUS.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
An enzyme found predominantly in platelet microsomes. It catalyzes the conversion of PGG(2) and PGH(2) (prostaglandin endoperoxides) to thromboxane A2. EC
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
A preparation consisting of PLATELETS concentrated in a limited volume of PLASMA. This is used in various surgical tissue regeneration procedures where the GROWTH FACTORS in the platelets enhance wound healing and regeneration.
Blood clot formation in any part of the CAROTID ARTERIES. This may produce CAROTID STENOSIS or occlusion of the vessel, leading to TRANSIENT ISCHEMIC ATTACK; CEREBRAL INFARCTION; or AMAUROSIS FUGAX.
A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.
A genus of venomous snakes of the subfamily Crotalinae. Twelve species of this genus are found in North and Central America and Asia. Agkistrodon contortrix is the copperhead, A. piscivorus, the cottonmouth. The former is named for its russet or orange-brown color, the latter for the white interior of its mouth. (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, p336; Moore, Poisonous Snakes of the World, 1980, p75)
Retraction of a clot resulting from contraction of PLATELET pseudopods attached to FIBRIN strands. The retraction is dependent on the contractile protein thrombosthenin. Clot retraction is used as a measure of platelet function.
Condensed areas of cellular material that may be bounded by a membrane.
Elements of limited time intervals, contributing to particular results or situations.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Disorder characterized by a decrease or lack of platelet dense bodies in which the releasable pool of adenine nucleotides and 5HT are normally stored.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
Single-chain polypeptides of about 65 amino acids (7 kDa) from LEECHES that have a neutral hydrophobic N terminus, an acidic hydrophilic C terminus, and a compact, hydrophobic core region. Recombinant hirudins lack tyr-63 sulfation and are referred to as 'desulfato-hirudins'. They form a stable non-covalent complex with ALPHA-THROMBIN, thereby abolishing its ability to cleave FIBRINOGEN.
A family of related, adhesive glycoproteins which are synthesized, secreted, and incorporated into the extracellular matrix of a variety of cells, including alpha granules of platelets following thrombin activation and endothelial cells. They interact with a number of BLOOD COAGULATION FACTORS and anticoagulant factors. Five distinct forms have been identified, thrombospondin 1, -2, -3, -4, and cartilage oligomeric matrix protein (COMP). They are involved in cell adhesion, platelet aggregation, cell proliferation, angiogenesis, tumor metastasis, VASCULAR SMOOTH MUSCLE growth, and tissue repair.
Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
Any form of purpura in which the PLATELET COUNT is decreased. Many forms are thought to be caused by immunological mechanisms.
Compounds that bind to and block the stimulation of PURINERGIC P2 RECEPTORS.
Group of hemorrhagic disorders in which the VON WILLEBRAND FACTOR is either quantitatively or qualitatively abnormal. They are usually inherited as an autosomal dominant trait though rare kindreds are autosomal recessive. Symptoms vary depending on severity and disease type but may include prolonged bleeding time, deficiency of factor VIII, and impaired platelet adhesion.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
Hemorrhagic and thrombotic disorders that occur as a consequence of abnormalities in blood coagulation due to a variety of factors such as COAGULATION PROTEIN DISORDERS; BLOOD PLATELET DISORDERS; BLOOD PROTEIN DISORDERS or nutritional conditions.
A thrombin receptor subtype that couples to HETEROTRIMERIC GTP-BINDING PROTEINS resulting in the activation of a variety of signaling mechanisms including decreased intracellular CYCLIC AMP, increased TYPE C PHOSPHOLIPASES and increased PHOSPHOLIPASE A2.
Bleeding or escape of blood from a vessel.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
Cell surface receptors that bind prostaglandins with high affinity and trigger intracellular changes which influence the behavior of cells. Prostaglandin receptor subtypes have been tentatively named according to their relative affinities for the endogenous prostaglandins. They include those which prefer prostaglandin D2 (DP receptors), prostaglandin E2 (EP1, EP2, and EP3 receptors), prostaglandin F2-alpha (FP receptors), and prostacyclin (IP receptors).
Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).
The number of LEUKOCYTES and ERYTHROCYTES per unit volume in a sample of venous BLOOD. A complete blood count (CBC) also includes measurement of the HEMOGLOBIN; HEMATOCRIT; and ERYTHROCYTE INDICES.
A group of physiologically active prostaglandin endoperoxides. They are precursors in the biosynthesis of prostaglandins and thromboxanes. The most frequently encountered member of this group is the prostaglandin H2.
The physiologically active and stable hydrolysis product of EPOPROSTENOL. Found in nearly all mammalian tissue.
Adherence of cells to surfaces or to other cells.
A familial coagulation disorder characterized by a prolonged bleeding time, unusually large platelets, and impaired prothrombin consumption.
Precursors in the biosynthesis of prostaglandins and thromboxanes from arachidonic acid. They are physiologically active compounds, having effect on vascular and airway smooth muscles, platelet aggregation, etc.
Amidines substituted with a benzene group. Benzamidine and its derivatives are known as peptidase inhibitors.
Proteins prepared by recombinant DNA technology.
A potent vasodilator agent that increases peripheral blood flow.
Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.
Venoms from SNAKES of the viperid family. They tend to be less toxic than elapid or hydrophid venoms and act mainly on the vascular system, interfering with coagulation and capillary membrane integrity and are highly cytotoxic. They contain large amounts of several enzymes, other factors, and some toxins.
The natural enzymatic dissolution of FIBRIN.
An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports CALCIUM and other divalent cations across membranes and uncouples oxidative phosphorylation while inhibiting ATPase of rat liver mitochondria. The substance is used mostly as a biochemical tool to study the role of divalent cations in various biological systems.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.
A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, pre-eclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders.
Collagen receptors are cell surface receptors that modulate signal transduction between cells and the EXTRACELLULAR MATRIX. They are found in many cell types and are involved in the maintenance and regulation of cell shape and behavior, including PLATELET ACTIVATION and aggregation, through many different signaling pathways and differences in their affinities for collagen isoforms. Collagen receptors include discoidin domain receptors, INTEGRINS, and glycoprotein VI.
A class of cell surface receptors for PURINES that prefer ATP or ADP over ADENOSINE. P2 purinergic receptors are widespread in the periphery and in the central and peripheral nervous system.
A sulfur-containing alkyl thionitrite that is one of the NITRIC OXIDE DONORS.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
A lipoxygenase metabolite of ARACHIDONIC ACID. It is a highly selective ligand used to label mu-opioid receptors in both membranes and tissue sections. The 12-S-HETE analog has been reported to augment tumor cell metastatic potential through activation of protein kinase C. (J Pharmacol Exp Ther 1995; 274(3):1545-51; J Natl Cancer Inst 1994; 86(15):1145-51)
A family of polypeptides purified from snake venoms, which contain the arginine-glycine-aspartic acid (RGD) sequence. The RGD tripeptide binds to integrin receptors and thus competitively inhibits normal integrin-ligand interactions. Disintegrins thus block adhesive functions and act as platelet aggregation inhibitors.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
Increased numbers of platelets in the peripheral blood. (Dorland, 27th ed)
A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
A humoral factor that stimulates the production of thrombocytes (BLOOD PLATELETS). Thrombopoietin stimulates the proliferation of bone marrow MEGAKARYOCYTES and their release of blood platelets. The process is called THROMBOPOIESIS.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed)
Chemically stimulated aggregation of cell surface receptors, which potentiates the action of the effector cell.
Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.
An integrin beta subunit of approximately 85-kDa in size which has been found in INTEGRIN ALPHAIIB-containing and INTEGRIN ALPHAV-containing heterodimers. Integrin beta3 occurs as three alternatively spliced isoforms, designated beta3A-C.
Solutions or mixtures of toxic and nontoxic substances elaborated by snake (Ophidia) salivary glands for the purpose of killing prey or disabling predators and delivered by grooved or hollow fangs. They usually contain enzymes, toxins, and other factors.
DITERPENES with three LACTONES and a unique tert-butyl group, which are found in GINKGO plants along with BILOBALIDES.
Blood-coagulation factor VIII. Antihemophilic factor that is part of the factor VIII/von Willebrand factor complex. Factor VIII is produced in the liver and acts in the intrinsic pathway of blood coagulation. It serves as a cofactor in factor X activation and this action is markedly enhanced by small amounts of thrombin.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
Agents that prevent clotting.
The residual portion of BLOOD that is left after removal of BLOOD CELLS by CENTRIFUGATION without prior BLOOD COAGULATION.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Proteins and peptides found in SALIVA and the SALIVARY GLANDS. Some salivary proteins such as ALPHA-AMYLASES are enzymes, but their composition varies in different individuals.
A purely physical condition which exists within any material because of strain or deformation by external forces or by non-uniform thermal expansion; expressed quantitatively in units of force per unit area.
Microscopy in which the object is examined directly by an electron beam scanning the specimen point-by-point. The image is constructed by detecting the products of specimen interactions that are projected above the plane of the sample, such as backscattered electrons. Although SCANNING TRANSMISSION ELECTRON MICROSCOPY also scans the specimen point by point with the electron beam, the image is constructed by detecting the electrons, or their interaction products that are transmitted through the sample plane, so that is a form of TRANSMISSION ELECTRON MICROSCOPY.
An integrin alpha subunit that primarily combines with INTEGRIN BETA1 to form the INTEGRIN ALPHA2BETA1 heterodimer. It contains a domain which has homology to collagen-binding domains found in von Willebrand factor.
The sum of the weight of all the atoms in a molecule.
A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.
Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.
A layer of epithelium that lines the heart, blood vessels (ENDOTHELIUM, VASCULAR), lymph vessels (ENDOTHELIUM, LYMPHATIC), and the serous cavities of the body.
The internal resistance of the BLOOD to shear forces. The in vitro measure of whole blood viscosity is of limited clinical utility because it bears little relationship to the actual viscosity within the circulation, but an increase in the viscosity of circulating blood can contribute to morbidity in patients suffering from disorders such as SICKLE CELL ANEMIA and POLYCYTHEMIA.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Clotting time of PLASMA recalcified in the presence of excess TISSUE THROMBOPLASTIN. Factors measured are FIBRINOGEN; PROTHROMBIN; FACTOR V; FACTOR VII; and FACTOR X. It is used for monitoring anticoagulant therapy with COUMARINS.
The ability of a substance to be dissolved, i.e. to form a solution with another substance. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
A fibrous protein complex that consists of proteins folded into a specific cross beta-pleated sheet structure. This fibrillar structure has been found as an alternative folding pattern for a variety of functional proteins. Deposits of amyloid in the form of AMYLOID PLAQUES are associated with a variety of degenerative diseases. The amyloid structure has also been found in a number of functional proteins that are unrelated to disease.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
Coagulant substances inhibiting the anticoagulant action of heparin.
The process of generating thrombocytes (BLOOD PLATELETS) from the pluripotent HEMATOPOIETIC STEM CELLS in the BONE MARROW via the MEGAKARYOCYTES. The humoral factor with thrombopoiesis-stimulating activity is designated THROMBOPOIETIN.
Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
A deficiency or absence of FIBRINOGEN in the blood.
A uricosuric drug that is used to reduce the serum urate levels in gout therapy. It lacks anti-inflammatory, analgesic, and diuretic properties.
An integrin found on fibroblasts, platelets, endothelial and epithelial cells, and lymphocytes where it functions as a receptor for COLLAGEN and LAMININ. Although originally referred to as the collagen receptor, it is one of several receptors for collagen. Ligand binding to integrin alpha2beta1 triggers a cascade of intracellular signaling, including activation of p38 MAP kinase.
Processes involved in the formation of TERTIARY PROTEIN STRUCTURE.
The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of BLOOD COAGULATION. It is used as a screening test and to monitor HEPARIN therapy.
A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752)
A family of snakes comprising three subfamilies: Azemiopinae (the mountain viper, the sole member of this subfamily), Viperinae (true vipers), and Crotalinae (pit vipers). They are widespread throughout the world, being found in the United States, Central and South America, Europe, Asia and Africa. Their venoms act on the blood (hemotoxic) as compared to the venom of elapids which act on the nervous system (neurotoxic). (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, pp333-36)
Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
The diversion of RADIATION (thermal, electromagnetic, or nuclear) from its original path as a result of interactions or collisions with atoms, molecules, or larger particles in the atmosphere or other media. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Physiologically active prostaglandins found in many tissues and organs. They show pressor activity, are mediators of inflammation, and have potential antithrombotic effects.
Compounds obtained by chemical synthesis that are analogs or derivatives of naturally occurring prostaglandins and that have similar activity.
The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.
The time required by whole blood to produce a visible clot.
2-Octylcyclopentaneheptanoic acids. The family of saturated carbon-20 cyclic fatty acids that represent the parent compounds of the prostaglandins.
(11 alpha,13E,15S)-11,15-Dihydroxy-9-oxoprost-13-en-1-oic acid (PGE(1)); (5Z,11 alpha,13E,15S)-11,15-dihydroxy-9-oxoprosta-5,13-dien-1-oic acid (PGE(2)); and (5Z,11 alpha,13E,15S,17Z)-11,15-dihydroxy-9-oxoprosta-5,13,17-trien-1-oic acid (PGE(3)). Three of the six naturally occurring prostaglandins. They are considered primary in that no one is derived from another in living organisms. Originally isolated from sheep seminal fluid and vesicles, they are found in many organs and tissues and play a major role in mediating various physiological activities.
Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis.
The action of a drug in promoting or enhancing the effectiveness of another drug.
Disruption of the non-covalent bonds and/or disulfide bonds responsible for maintaining the three-dimensional shape and activity of the native protein.
A subclass of phospholipases that hydrolyze the phosphoester bond found in the third position of GLYCEROPHOSPHOLIPIDS. Although the singular term phospholipase C specifically refers to an enzyme that catalyzes the hydrolysis of PHOSPHATIDYLCHOLINE (EC, it is commonly used in the literature to refer to broad variety of enzymes that specifically catalyze the hydrolysis of PHOSPHATIDYLINOSITOLS.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
An eicosanoid, derived from the cyclooxygenase pathway of arachidonic acid metabolism. It is a stable and synthetic analog of EPOPROSTENOL, but with a longer half-life than the parent compound. Its actions are similar to prostacyclin. Iloprost produces vasodilation and inhibits platelet aggregation.
The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Two small peptide chains removed from the N-terminal segment of the alpha chains of fibrinogen by the action of thrombin during the blood coagulation process. Each peptide chain contains 18 amino acid residues. In vivo, fibrinopeptide A is used as a marker to determine the rate of conversion of fibrinogen to fibrin by thrombin.
A synuclein that is a major component of LEWY BODIES that plays a role in neurodegeneration and neuroprotection.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
Monomeric subunits of primarily globular ACTIN and found in the cytoplasmic matrix of almost all cells. They are often associated with microtubules and may play a role in cytoskeletal function and/or mediate movement of the cell or the organelles within the cell.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
The volume of packed RED BLOOD CELLS in a blood specimen. The volume is measured by centrifugation in a tube with graduated markings, or with automated blood cell counters. It is an indicator of erythrocyte status in disease. For example, ANEMIA shows a low value; POLYCYTHEMIA, a high value.
An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.
Compounds and molecular complexes that consist of very large numbers of atoms and are generally over 500 kDa in size. In biological systems macromolecular substances usually can be visualized using ELECTRON MICROSCOPY and are distinguished from ORGANELLES by the lack of a membrane structure.
Fatty acid derivatives of glycerophosphates. They are composed of glycerol bound in ester linkage with 1 mole of phosphoric acid at the terminal 3-hydroxyl group and with 2 moles of fatty acids at the other two hydroxyl groups.
A gram-positive organism found in dental plaque, in blood, on heart valves in subacute endocarditis, and infrequently in saliva and throat specimens. L-forms are associated with recurrent aphthous stomatitis.
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.
A family of transmembrane glycoproteins (MEMBRANE GLYCOPROTEINS) consisting of noncovalent heterodimers. They interact with a wide variety of ligands including EXTRACELLULAR MATRIX PROTEINS; COMPLEMENT, and other cells, while their intracellular domains interact with the CYTOSKELETON. The integrins consist of at least three identified families: the cytoadhesin receptors(RECEPTORS, CYTOADHESIN), the leukocyte adhesion receptors (RECEPTORS, LEUKOCYTE ADHESION), and the VERY LATE ANTIGEN RECEPTORS. Each family contains a common beta-subunit (INTEGRIN BETA CHAINS) combined with one or more distinct alpha-subunits (INTEGRIN ALPHA CHAINS). These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development; HEMOSTASIS; THROMBOSIS; WOUND HEALING; immune and nonimmune defense mechanisms; and oncogenic transformation.
Clotting time of PLASMA mixed with a THROMBIN solution. It is a measure of the conversion of FIBRINOGEN to FIBRIN, which is prolonged by AFIBRINOGENEMIA, abnormal fibrinogen, or the presence of inhibitory substances, e.g., fibrin-fibrinogen degradation products, or HEPARIN. BATROXOBIN, a thrombin-like enzyme unaffected by the presence of heparin, may be used in place of thrombin.

Primary haemostasis: sticky fingers cement the relationship. (1/4463)

Platelet aggregation to form a haemostatic plug, or thrombus, plays a key role in preventing bleeding from a wound. Recent studies have provided new insights into how platelet receptors are deployed during the interactions with the vascular subendothelial matrix that lead to haemostatic plug formation.  (+info)

Nitric oxide in the endometrium. (2/4463)

Nitric oxide (NO) is an important mediator of paracrine interactions, especially within the vascular system. It is a powerful inhibitor of platelet aggregation and a potent vasodilator. NO is also a neurotransmitter and it plays a role in cell-mediated cytotoxicity. NO-generating enzymes (nitric oxide synthases, NOS) have been described in the endometrium of a number of species, suggesting that NO might be involved in endometrial function. In human endometrium, endothelial NOS and inducible NOS have been localized to glandular epithelium in the non-pregnant uterus. Weak inducible NOS immunoreactivity has been observed in decidualized stromal cells. NO might participate in the initiation and control of menstrual bleeding. Furthermore, it may play a part in the inhibition of platelet aggregation within the endometrium, where menstrual haemostasis is thought to occur primarily by vasoconstriction rather than clot organization. Endometrially derived NO could also suppress myometrial contractility. Recent attention has focused on the part that NO might play in maintaining myometrial quiescence during pregnancy. NO also appears to relax the non-pregnant myometrium, an action which could be exploited for the medical treatment of primary dysmenorrhoea.  (+info)

Labeling of the internal pool of GP IIb-IIIa in platelets by c7E3 Fab fragments (abciximab): flow and endocytic mechanisms contribute to the transport. (3/4463)

Abciximab is a new antiplatelet therapeutic in ischemic cardiovascular disease. The drug, chimeric Fab fragments of a murine monoclonal antibody (MoAb) (c7E3), blocks GP IIb-IIIa function. However, its capacity to reach all receptor pools in platelets is unknown. Electron microscopy and immunogold labeling were used to localize abciximab in platelets of patients receiving the drug for up to 24 hours. Studies on frozen-thin sections showed that c7E3 Fab, in addition to the surface pool, also labeled the surface-connected canalicular system (SCCS) and alpha-granules. Analysis of gold particle distribution showed that intraplatelet labeling was not accumulative and in equilibrium with the surface pool. After short-term incubations of platelets with c7E3 Fab in vitro, gold particles were often seen in lines within thin elements of the SCCS, some of which appeared in contact with alpha-granules. Little labeling was associated with Glanzmann's thrombasthenia platelets, confirming that the channels contained bound and not free c7E3 Fab. Endocytosis of abciximab in clathrin-containing vesicles was visualized by double staining and constitutes an alternative mechanism of transport. The remaining free pool of GP IIb-IIIa was evaluated with the MoAb AP-2; flow cytometry showed it to be about 9% on the surface of nonstimulated platelets but 33% on thrombin-activated platelets. The ability of drugs to block all pools of GP IIb-IIIa and then to be associated with secretion-dependent residual aggregation must be considered when evaluating their efficiency in a clinical context.  (+info)

Activation of G12/G13 results in shape change and Rho/Rho-kinase-mediated myosin light chain phosphorylation in mouse platelets. (4/4463)

Platelets respond to various stimuli with rapid changes in shape followed by aggregation and secretion of their granule contents. Platelets lacking the alpha-subunit of the heterotrimeric G protein Gq do not aggregate and degranulate but still undergo shape change after activation through thromboxane-A2 (TXA2) or thrombin receptors. In contrast to thrombin, the TXA2 mimetic U46619 led to the selective activation of G12 and G13 in Galphaq-deficient platelets indicating that these G proteins mediate TXA2 receptor-induced shape change. TXA2 receptor-mediated activation of G12/G13 resulted in tyrosine phosphorylation of pp72(syk) and stimulation of pp60(c-src) as well as in phosphorylation of myosin light chain (MLC) in Galphaq-deficient platelets. Both MLC phosphorylation and shape change induced through G12/G13 in the absence of Galphaq were inhibited by the C3 exoenzyme from Clostridium botulinum, by the Rho-kinase inhibitor Y-27632 and by cAMP-analogue Sp-5,6-DCl-cBIMPS. These data indicate that G12/G13 couple receptors to tyrosine kinases as well as to the Rho/Rho-kinase-mediated regulation of MLC phosphorylation. We provide evidence that G12/G13-mediated Rho/Rho-kinase-dependent regulation of MLC phosphorylation participates in receptor-induced platelet shape change.  (+info)

Carbohydrate on human factor VIII/von Willebrand factor. Impairment of function by removal of specific galactose residues. (5/4463)

Human factor VIII/von Willebrand factor protein containing 120 +/- 12 nmol of sialic acid and 135 +/- 13 nmol of galactose/mg of protein was digested with neuraminidase. The affinity of native factor VIII/von Willebrand factor and its asialo form for the hepatic lectin that specifically binds asialoglycoproteins was assessed from in vitro binding experiments. Native factor VIII/von Willebrand factor exhibited negligible affinity while binding of the asialo derivative was comparable to that observed for asialo-alpha1-acid glycoprotein. Incubation of asialo-factor VIII/von Willebrand factor with Streptococcus pneumoniae beta-galactosidase removed only 62% of the galactose but abolished binding to the purified hepatic lectin. When the asialo derivative was incubated with purified beta-D-galactoside alpha2 leads to 6 sialyltransferase and CMP-[14C]NeuAc, only 61% of the galactose incorporated [14C]NeuAc. From the known specificites of these enzymes, it is concluded that galactose residues important in lectin binding are present in a terminal Gal/beta1 leads to 4GlcNAc sequence on asialo-factor VIII/von Willebrand factor. The relative ristocetin-induced platelet aggregating activity of native, asialo-, and agalacto-factor VIII/von Willebrand factor was 100:38:12, respectively, while procoagulant activity was 100:100:103.  (+info)

Effects of docosahexaenoic and eicosapentaenoic acid on lipid metabolism, eicosanoid production, platelet aggregation and atherosclerosis in hypercholesterolemic rats. (6/4463)

Exogenously hypercholesterolemic (ExHC) rats were fed on an atherogenic diet supplemented with 1% each of either ethyl ester docosahexaenoic acid [EE-DHA, 22:6(n-3)], ethyl ester eicosapentaenoic acid [EE-EPA, 20:5(n-3)] or safflower oil (SO) for 6 months. The rats fed on the diets containing EE-EPA or EE-DHA, compared with those fed on SO, had lower serum cholesterol and triacylglycerol levels, less aggregation of platelets and slower progress of intimal thickening in the ascending aorta. Relative to the SO-fed rats, both of the (n-3) fatty acid-fed rats had a significantly reduced proportion of arachidonic acid in the platelet and aortic phospholipids, and lower production of thromboxane A2 by platelets and of prostacyclin by the aorta. These results suggest that EPA and DHA are similarly involved in preventing atherosclerosis development by reducing hypercholesterolemia and modifying the platelet functions.  (+info)

Platelet aggregation and incident ischaemic heart disease in the Caerphilly cohort. (7/4463)

BACKGROUND: Platelets are involved in myocardial infarction but evidence of prediction of infarction by measures of platelet function are sparce. METHODS: Platelet aggregation to thrombin and to ADP in platelet rich plasma was recorded for 2176 men aged 49-65 years in the Caerphilly cohort study. RESULTS: Results from 364 men were excluded, 80 of whom had not fasted before venepuncture; most of the others were excluded because antiplatelet medication had been taken shortly before the platelet tests. During the five years following the platelet tests 113 ischaemic heart disease (IHD) events which fulfilled the World Health Organisation criteria were identified--42 fatal and 71 non-fatal. No measure of platelet aggregation was found to be significantly predictive of incident IHD. The possibility that platelet function is predictive for only a limited time after it is characterised, and that prediction falls off with time, was tested. When IHD events are grouped by their time of occurrence after aggregation had been measured, the test results show a gradient suggestive of prediction of early IHD events. Thus, 24% of the men who had an event within 500 days of the test had had a high secondary response to ADP while only 12% of those whose IHD event had been 1000 or more days after the test had shown a high platelet response at baseline. The trend in these proportions is not significant. CONCLUSIONS: Platelet aggregation to thrombin and ADP in platelet rich plasma was recorded in the Caerphilly cohort study. No measure of aggregation was found to be predictive of IHD.  (+info)

Age-related changes in blood coagulation and fibrinolysis in mice fed on a high-cholesterol diet. (8/4463)

To investigate the pathogenesis of hyperlipidemia-induced atherosclerosis, we examined age-dependent changes in platelet activity, blood coagulation and fibrinolysis in susceptibility to a high cholesterol diet (HCD) feeding in male ICR mice. Pretreatment of platelet-rich-plasma from HCD feeding mice for 3 days with epinephrine (300 microM) resulted in a marked enhancement of adenosine 5'-diphosphate (ADP: 0.1 microM) or collagen (0.7 microgram/ml)-stimulated aggregation compared with the same in control mice. Yohimbine as alpha 2-adrenergic blocker antagonized these aggregations in a dose-dependent manner. A significant increase in plasma total cholesterol and VLDL (very low-density lipoprotein)-LDL (low-density lipoprotein)-cholesterol and the liver/body weight ratio was observed in mice fed on HCD for 3 months (3-month HCD mice). In the early phase of this experiment, a significant increase in fibrinogen was observed. In the middle phase, increases in the activity of antithrombin III (ATIII) and alpha 2-plasmin inhibitor (alpha 2-Pl) followed. Plasminogen content gradually decreased in both normal diet and HCD mice throughout the experiment. The activity of plasminogen activator inhibitor (PAI) decreased in 3-month HCD mice. Morphological observation of the aortic arch from 3-month HCD mice revealed apparent atheromatous plaques not seen in control mice. These results suggest that 3-month HCD mice can be a convenient hyperlipidemia-induced atherosclerotic model and the changes in platelet activity, coagulation and fibrinolysis in the early phase may be a cause of pathologic changes in this model.  (+info)

Patients will be consented for the study and asked to initial on the consent form to state whether they agree for the genetic testing. after signing informed consent, complete medical history and medication list will be obtained and verified with the ePiC electronic medical record. Patients will be screened for depression to make sure that they are not depressed. after meeting all inclusion and exclusion criteria during the screening visit, those patients on aspirin for primary prevention of CV events will be asked to stop it for 2 weeks prior to blood collection for baseline data. normal controls will be chosen after frequency matching for decade of age, gender, diabetes mellitus and interval of body mass index (5 kg/m2). Dietary supplements (Vitamin e and fish oil) known to affect platelet function will be assessed and patients on those will be asked to discontinue these. Participants with also be asked to not eat foods known to affect platelet function (coffee, chocolate, grapes, and alcohol) ...
Patients will be consented for the study and asked to initial on the consent form to state whether they agree for the genetic testing. After signing informed consent, complete medical history and medication list will be obtained and verified with the electronic medical record. After meeting all inclusion and exclusion criteria during the screening visit, those patients on aspirin for primary prevention of cardiovascular events will be asked to stop it for 2 weeks prior to blood collection for baseline data. Normal controls will be chosen after frequency matching for decade of age, gender, diabetes mellitus and interval of body mass index (5 kg/m2). Dietary supplements (Vitamin E and fish oil) known to affect platelet function will be assessed and patients on those will be asked to discontinue these. Participants with also be asked to not eat foods known to affect platelet function (coffee, chocolate, grapes, and alcohol) 48 hours prior to sample collection on visit 1. An interviewer-administered ...
Patients will be consented for the study and asked to initial on the consent form to state whether they agree for the genetic testing. After signing informed consent, complete medical history and medication list will be obtained and verified with the electronic medical record. After meeting all inclusion and exclusion criteria during the screening visit, those patients on aspirin for primary prevention of cardiovascular events will be asked to stop it for 2 weeks prior to blood collection for baseline data. Normal controls will be chosen after frequency matching for decade of age, gender, diabetes mellitus and interval of body mass index (5 kg/m2). Dietary supplements (Vitamin E and fish oil) known to affect platelet function will be assessed and patients on those will be asked to discontinue these. Participants with also be asked to not eat foods known to affect platelet function (coffee, chocolate, grapes, and alcohol) 48 hours prior to sample collection on visit 1. An interviewer-administered ...
The thienopyridine anti-platelet drugs, such as clopidogrel, require metabolic activation in vivo to effectively block platelet aggregation. The study of the activation of these compounds has been hampered by the lability and reactivity of the ring-opened active metabolite. Many studies have relied solely on the disappearance of the parent drug as an indicator of bioactivation by a particular cytochrome P450 (CYP). We have developed an alternative method for studying the formation of the active metabolite. Conditions were optimized whereby washed human platelets can be incubated in the presence of an individual, recombinant CYP and clopidogrel. At various time points during this incubation, an aliquot is removed and platelet aggregation is measured using 2-(Methylthio)adenosine 5′-diphosphate (2MeSADP) or adenosine 5′-diphosphate (ADP) as the agonist. Inhibition of platelet aggregation, compared to the control lacking active enzyme, suggests the formation of the thienopyridine active ...
The present study clarifies several aspects of the effects on platelet aggregation of arising and assuming the upright posture in the morning: 1) On arising, increased platelet aggregation can readily be observed in whole blood; 2) this increased aggregation is not accompanied by platelet activation, as evidenced by changes in activation-dependent markers on the platelet surface; 3) the observed increase in aggregation in whole blood may be partly explained by increases in platelet count and hematocrit that accompany arising. In addition, the study confirmed previous reports of increased fibrinolysis on standing and provided new evidence of an opposing increase in thrombin generation on standing.. Comparison with previous studies. Studies reporting the effects of arising in the morning on platelet aggregation (7-11,13) have exclusively studied aggregation in PRP, and to our knowledge, the present study is the first to report the effects of arising on platelet aggregation in whole blood. Of the ...
TY - JOUR. T1 - A study of whole blood platelet and white cell aggregation using a laser flow aggregometer. AU - Sun, J.. AU - Abel, E. W.. AU - Bancroft, A.. AU - McLaren, M.. AU - Belch, J. J. F.. PY - 2003. Y1 - 2003. N2 - Both platelet aggregation and white blood cell aggregation are involved in pathological processes such as thrombosis, atherosclerosis and chronic inflammation. People in older age groups are likely to suffer from cardiovascular diseases and may have increased white cell and platelet aggregation which could contribute to this increased risk. This study aimed to compare white cell and platelet aggregation between different age and gender groups. Whole blood white cell aggregation and platelet aggregation were carried out on healthy volunteers using cytometric techniques. It was found that both white cell and platelet aggregation in the elderly group (white cell aggregation median value, 0.08; range, 0.02-0.14; platelet aggregation median value, 0.32; range, 0.1-0.39) were ...
BioAssay record AID 336312 submitted by ChEMBL: Antiplatelet activity against bovine citreated platelet assessed as inhibition of ADP-induced platelet aggregation up to 278 ug/ml after 6 mins.
A series of nonsteroidal anti-inflammatory drugs (NSAIDs) [S(+)-naproxen, ibuprofen isomers, and indomethacin] were evaluated for their activation of peroxisome proliferator-activated receptor (PPAR) α and γ isoforms in CV-1 cells co-transfected with rat PPAR α and γ, and peroxisome proliferator response element (PPRE)-luciferase reporter gene plasmids, for stimulation of peroxisomal fatty acyl CoA β-oxidase activity in H4IIEC3 cells, and for comparative inhibition of ovine prostaglandin endoperoxide H synthase (PGHS)-1 and PGHS-2 and arachidonic acid-induced human platelet activation. Each drug produced a concentration-dependent activation of the PPAR isoforms and fatty acid β-oxidase activity, inhibition of human arachidonic acid-induced platelet aggregation and serotonin secretion, and inhibition of PGHS-1 and PGHS-2 activities. For PPARα activation in CV-1 and H4IIEC3 cells, and the stimulation of fatty acyl oxidase activity in H4IIEC3 cells, the rank order of stereoselectivity was ...
This study was conducted to examine the mechanism(s) of synergistic interaction of adrenaline and platelet-activating factor (PAF) mediated human platelet aggregation. We found that platelet aggregation mediated by subthreshold concentrations of PAF (5-8 nM) plus adrenaline (0.5-2 μM) was inhibited by both α2-adrenoceptor blocker (yohimbine) and PAF receptor antagonist (WEB2086). While examining the role of the downstream signalling pathways, we found that this synergism was inhibited by calcium channel blockers, verapamil, and diltiazem. In addition, platelet aggregation by co-addition of adrenaline and PAF was also inhibited by very low concentrations of phospholipase C (PLC) inhibitor (U73122; IC50 = 0.2 μM), the MAP kinase inhibitor, PD98059 (IC50 = 3 μM) and cyclooxygenase (COX-1) inhibitors including indomethacin (IC50 = 0.25 μM), flurbiprofen (IC50 = 0.7 μM) and piroxicam (IC50 = 7 μM). However, the COX-2 inhibitor, nimesulide, was also effective in inhibiting the aggregation. The
The work herein examines in vitro platelet aggregation in response to fluid shearing motion. Our specific aim is to characterize shear-induced aggregation by means of kinetic measurements. In doing so we consider plausible physicochemical mechanisms for platelet activation in the shear field. Besides resolving some questions concerning the activation of platelets by shear forces, this study further implicates fluid mechanical factors in thrombosis and arterial disease. Specific results may also apply to the design and evaluation of blood-contacting artificial devices. The experimental procedure centers on the use of a rotational viscometer to apply a controlled shearing motion to platelet suspensions for prescribed times. We quantify aggregation through changes in particle size histograms and associated measures (e.g. total number of particles). Additional insight into the aggregation response comes from interpreting kinetic data using the coalescence equation, a population balance specific for ...
Major Depressive Disorder (MDD) can lead to adverse cardiovascular outcomes in patients with chronic kidney disease (CKD). Although one of the proposed mechanisms is heightened platelet activation, effects of MDD and its treatment with a selective serotonin reuptake inhibitor (SSRI) on platelet function in patients with CKD remain unclear. In a pre-specified analysis, changes from baseline to 12 weeks in whole blood platelet aggregation (WBPA) and plasma levels of E-selectin and P-selectin on treatment with sertraline vs. placebo were investigated in 175 patients with CKD (estimated glomerular filtration rate [eGFR] | 60 ml/min/1.73m2) and MDD (MDD+/CKD+) in a randomized, double-blind trial. Correlations between severity of depressive symptoms and platelet function were also analyzed. In order to investigate whether differences in platelet function were due to presence of CKD or MDD, we compared a subgroup of 49 MDD+/CKD+ patients with eGFR | 30 ml/min/1.73m2 to 43 non-depressed CKD controls (28 CKD
Many vegetables contain omega-3 fats, including cauliflower, collard greens, romaine lettuce, broccoli, kale and cabbage. Some vegetables also contain salicylates, which are found in aspirin and thin the blood to prevent clotting. Salicylates occur naturally in cucumbers, alfalfa, mushrooms, radishes and zucchini, notes WebMD. According to the Worlds Healthiest Foods website, the Journal of the American Medical Association research suggests that tomato juice may decrease platelet aggregation. The study focused on the effects of tomato juice on people with type 2 diabetes. When choosing tomato juice, opt for the low-sodium varieties. ...
INTRODUCTION. Cardiopulmonary bypass (CPB) affects platelets, and platelet dysfunction is considered to be an important risk factor for post-operative bleeding after coronary artery bypass graft (CABG) surgery. Monitoring platelet function in the peri-operative period therefore is of importance to reduce morbidity due to both bleeding and post-operative graft occlusion. Our aim was to study platelet reactivity in CABG patients in the peri-operative period.. METHODS. Platelet function in 30 patients undergoing CABG was analyzed using an impedance aggregometry point-of-care (POC) instrument (Multiplate). Platelet reactivity was measured preoperatively at induction of anaesthesia, preoperatively immediately before CPB, after 30 minutes of CPB, after end of CPB, postoperatively at arrival to the ICU and finally at 3 and 18 h after surgery. Whole blood platelet aggregation was measured after activation with ADP (adenosin diphosphate), TRAP (thrombin receptor activating peptide), AA (arachidonic acid) ...
Comparison of platelet fibronectin, ADP-induced platelet aggregation and serum total nitric oxide (NOx) levels in angiographically determined coronary artery disease ...
We describe the first comparison of the effects of antagonists of different integrins on the arterial response to injury. These data indicate that continuous infusions of antagonists of either αIIbβ3 or αvβ3, started before and continued for 2 weeks after porcine PTCA, significantly reduce neointima formation at 28 days. αIIbβ3 inhibitors had marked effects on platelet aggregation and thrombus formation 6 hours after PTCA, whereas a selective αvβ3 inhibitor showed no effect. Equally, the αvβ3 inhibitors were able to inhibit VSMC adhesion, a property not shared by the selective αIIbβ3 inhibitor, although final reductions in neointima were comparable between the 3 treatment groups.. Both αIIbβ3 inhibition and combined αIIbβ3/αvβ3 inhibition induced rapid inhibition of ex vivo platelet aggregation, translating into concomitant reductions in adherent thrombus. Measurement of ex vivo platelet aggregation may overestimate the degree of platelet inhibition, and the relevance of this ...
Pharmacodynamic assessment. to determine the dose of clopidogrel to achieve a mean 30-50% inhibition of ADP-induced platelet aggregation in neonates or
Hart Biologicals Epinephrine Reagent is used to diagnose platelet dysfunction, or normal platelet activity in human platelet rich plasma or whole blood.. The platelet aggregation test measures the rate and degree to which dispersed platelets in a sample of platelet rich plasma (PRP) or anti-coagulated whole blood forms clumps (aggregates) after the addition of a substance that normally stimulates platelet aggregation (agonist). Epinephrine can stimulate fibrinogen binding and platelet aggregation without causing platelet secretion, however as is the case with other so called weak agonists, platelet secretion in response to Epinephrine takes place only after initial aggregation.. Hart Biologicals Epinephrine Reagent is supplied as the following for reconstitution with 1.0ml distilled water:. · 1 x 1.0ml 100uM Epinephrine. Note: To download a copy of this Products Instructions For Use in English, create an account by clicking Register at the top right corner of this screen. Other European ...
In their original description of PEAR1, Nanda et al17 demonstrated that platelet activation and initial contact induced by thrombin or collagen resulted in tyrosine phosphorylation of PEAR1, and that this could be inhibited by eptifibatide, a GPIIb/IIIa inhibitor. Platelet function was not assessed. Our results are the first to show that PEAR1 contributes significantly to maximal aggregation induced by collagen or epinephrine in native platelets, as well as to responsiveness of platelets to aspirin, in both whites and blacks.. Our study demonstrates that the CC genotype of rs2768759 in the PEAR1 gene is associated with higher levels of residual platelet aggregation to collagen, epinephrine, and ADP after low dose aspirin, consistent with greater platelet reactivity. The CC genotype was also associated with greater native platelet aggregation, but the results were less pronounced and less consistent. Consistent with these results, the aspirin response phenotype (postaspirin aggregation adjusted ...
Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation.. ...
Minami N, Suzuki Y, Yamamoto M, Kihira H, Imai E, Wada H, Kimura Y, Ikeda Y, Shiku H, Nishikawa M.; Inhibition of shear stress-induced platelet aggregation by cilostazol, a specific inhibitor of cGMP-inhibited phosphodiesterase, in vitro and ex vivo.; Life Sci. , 1997 PubMed Europe PMC ...
The objective of this work was to further our understanding of the influence hemodynamic forces have on the cardiovascular system. Specifically, the effect of shear stress on platelet aggregability under two pathophysiological conditions was studied. Elevated shear stress levels in stenosed vessels induce platelet aggregation. Increased plasma catecholamine concentrations have also been implicated in the onset of acute coronary ischemic syndromes. This first study was designed to examine the synergistic platelet activation by the interaction of shear stress and epinephrine. Platelets suspensions sheared at subthreshold levels in a cone and plate viscometer showed little or no aggregation unless pretreated with subthreshold concentrations of epinephrine. Monoclonal antibody blockade of glycoproteins (Gp) Ib and IIb/IIIa showed that the synergistic platelet aggregation required functional Gp IIb/IIIa but could partially bypass Gp Ib-von Willebrand factor (vWF) interaction. Binding studies ...
Normal primary platelet aggregation requires agonist-mediated activation of membrane GPIIb-IIIa, binding of fibrinogen to GPIIb-IIIa, and cellular events after ligand binding. PAC1 monoclonal antibody distinguishes between resting and activated states of GPIIb-IIIa, and other antibodies preferentially recognize GPIIb (PMI-1) or IIIa (anti-LIBS1) after the binding of fibrinogen or fibrinogen-mimetic peptides, such as GRGDSP. Using these antibodies and platelet flow cytometry, we studied two distinct persistent platelet aggregation abnormalities. Platelets from a thrombasthenic variant, which contained near-normal amounts of GPIIb-IIIa, failed to aggregate or bind PAC1 in response to agonists. In addition, GRGDSP, which binds to normal GPIIb-IIIa without prior cell activation, failed to increase the binding of PMI-1 or anti-LIBS1 to the thrombasthenic platelets, suggesting a primary defect in ligand binding. Chromatography of detergent-solubilized platelets on a KYGRGDS affinity column confirmed ...
The platelet aggregation blood test checks how well platelets, a part of blood, clump together and cause blood to clot. Learn more about this test here.
TY - JOUR. T1 - Functional alterations of human platelets following 111In labeling with different ligands and incubation media. AU - Mieno, M.. AU - Isaka, Y.. AU - Kimura, K.. AU - Matsumoto, M.. AU - Etani, H.. AU - Uehara, A.. AU - Hashikawa, K.. AU - Hata, R.. AU - Moriwaki, H.. AU - Ashida, K.. AU - Imaizumi, M.. AU - Kamada, T.. AU - Kozuka, T.. PY - 1990/1/1. Y1 - 1990/1/1. N2 - We studied the effects of various 111In-water soluble chelates and incubation media on labeling efficiency of platelets and in vitro platelet aggregability. High labeling efficiency of platelets in ACD-saline was achieved with 111In-oxine sulfate, 111In-tropolone and 111In-MPO (2-mercaptopyridine-N-oxide). In the condition with 4.8 x 106/mm3 platelets in ACD-plasma, 111In-oxine-sulfate had low labeling efficiency and inconsistent labeling, while 111In-tropolone and 111In-MPO had high labeling efficiency. In vitro platelet aggregability (ADP 2 μM) was reduced when platelets were labeled in the absence of plasma. ...
This article discusses the advantages and disadvantages of methods for the measurement of platelet function. The focus is on tests that can be used to monitor antiplatelet activity in the setting of cardiovascular disease and potentially predict thrombosis and bleeding. The tests described are platelet aggregometry; impedance aggregometry; VerifyNow (Accumetrics, San Diego, CA); Plateletworks (Helena Laboratories, Beaumont, TX); platelet surface P-selectin, platelet surface-activated glycoprotein IIb/IIIa, and leukocyte-platelet aggregates; TEG Platelet Mapping system (Haemoscope, Niles, IL); Impact cone and plate(let) analyzer (DiaMed, Cressier, Switzerland); Platelet Function Analyzer-100 (Siemens Healthcare Diagnostics, Inc., Deerfield, IL); phosphorylation of vasodilator-stimulated phosphoprotein; serum thromboxane B(2); and urinary 11-dehydro thromboxane B(2). Some of the factors that differentiate these tests are sample volume requirements, the use of whole blood, the presence of shear, point-of
Results: 22 hypoxemic patients were selected for the study based on their diagnosis of COPD (from history and spirometry) along with age and sex matched controls. Presence of comorbidities and other factors that cause platelet activation were excluded. Level of platelet aggregation was determined by several experiments. By an aggregometer using platelet agonists (thrombin and ADP) it was found that platelet aggregation was significantly higher in hypoxemic COPD patients than normal healthy controls. Fluorescence spectrophotometer was used to measure intracellular calcium as a marker of platelet activation and it was found that hypoxemic COPD patients had significantly higher platelet aggregation than normal healthy controls. However no significant difference was found in other markers of platelet activation studied namely P-selectin exposure and PAC-1 binding between the two groups ...
Human platelets express Toll-like receptors (TLR) 4. However, the mechanism by which TLR4 directly affects platelet aggregation and blood coagulation remains to be explored. Therefore, in this study, we evaluated the platelet TLR4 expression in patients who underwent CABG surgery; we explored the correlation between platelet TLR4 expression and the early outcomes in hospital of patients. Additionally, C57BL/6 and C57BL/6-|i|Tlr|/i||sup||i|LPS|/i|−/−|/sup| mice were used to explore the roles of platelet TLR4 in coagulation by platelet aggregometry and rotation thromboelastometry. In conclusion, our results highlight the important roles of TLR4 in blood coagulation and platelet function. Of clinical relevance, we also explored novel roles for platelet TLR4 that are associated with early outcomes in cardiac surgery.
We assessed the effect of local anesthetics (LA) from different families such as esters (benzocaine), linear aminoamides (lidocaine) and cyclic aminoamides (bupivacaine) on the platelet aggregation induced by ADP. Liposomal formulations of the three LA, prepared with egg phosphatidylcholine: cholesterol a-tocopherol, were also tested. The three LA were able to inhibit platelet aggregation induced by ADP, in the following order: bupivacaine , lidocaine , benzocaine. After encapsulation into liposomes the inhibitory effect increased for all anesthetics studied, showing that aggregation tests could be used to assess the toxicity of new drug formulations ...
Methods Blood was collected by venepuncture into 0.32% trisodium citrate. Platelet rich plasma (PRP) was isolated by centrifugation and either tested directly or further washed with Tyrodes-Hepes buffer. The PRP or washed platelets (WP) were incubated with the P2Y12 inhibitor prasugrel active metabolite (PAM; 3 µM) or vehicle (0.5% DMSO) for 30 min followed by 1 min incubation with the NO donor DEA/NONOate (10 nM-1 mM) and/or PGI2 (0.2 nM-100 nM) and/or vehicle (0.01M NaOH). WP platelet aggregation to thrombin (1U/ml) was measured by 96-well aggregometry and PRP platelet aggregation to TRAP-6 (Thrombin Receptor Activating Peptide-6, 30 µM) or collagen (30 µg/ml) was measured by light transmission aggregometry (LTA). Isobolograms were constructed by plotting the IC50 values for DEA-NONOate and PGI2 in vehicle or PAM treated WP. Data represents mean±SEM % final platelet aggregation from 4-5 healthy volunteers.⇓ ⇓ ...
The present study was performed in 34 patients with transient cerebral ischemia, TCI. Twenty-four of the patients were examined angiographically. Atherosclerotic abnormalities were demonstrated in 13 and a total occlusion of the interior carotid artery was found in one patient. The angiograms were normal in 10 patients. One patient suffered from hyperlipoproteinemia, type IV, and one from diabetes mellitus. The platelet aggregation in vitro was increased significantly, as more patients than normal controls showed secondary aggregation with low ADP-concentration: less than or equal to 1 mumol (p less than 0.001). The fibrinolytic capacity was significantly reduced (p less than 0.01) but not particularly in the patients with increased tendency for platelet aggregation. No correlation found between changes in platelet aggregation, the fibrinolytic activity and the angiographic findings. The results described may favor the concept that a prophylactic use of drug excerting an antiaggregation effect on
The second part of this thesis explores the suitability of the 96-well plate format to study platelet aggregation, and to assess inhibition, using aspirin and the P2Y12 antagonist, cangrelor. The 96-well plate format has successfully demonstrated dose-dependent inhibition of adenosine diphosphate (ADP)-induced platelet aggregation with cangrelor and of arachidonic acid (AA)-induced platelet aggregation with aspirin, except when using high concentrations of AA. The apparent failure of aspirin to inhibit AA-induced platelet aggregation at a high concentration could have been due to the fact that endogenous ADP, which may have leaked from red blood cells (RBCs), may have overcome the inhibition. Dual antiplatelet therapy, using aspirin in conjunction with cangrelor, has confirmed this explanation and also demonstrated that more inhibition is obtained when antiplatelet agents are used in pairs. When the glycoprotein (GP) IIb/IIIa antagonist MK-0852 was used to block the final aggregation pathway, it ...
Human platelet-rich plasma (PRP) was irradiated in vitro with a fiberoptic Nd:YAG laser-heated metal cap to study its effects on platelets. The energy of the laser was 5 and 10 watts with an irradiation time of 0, 3, 6, and 9 seconds and 14 watts with an irradiation time of 0, 3, 4, and 5 seconds, respectively. The irradiated PRPs were analyzed for platelet count, aggregation reaction, thromboxane (TX)B2 measurement and electron microscopy. Various degrees of decrease in platelet count were observed in all groups. Except the 5Wx3S group, the other groups showed an increase in the maximum aggregation rate of platelets, which corresponded to the enhancement of TXB2 formation. It was also demonstrated by a transmission electron microscopy in 10Wx3S, 10Wx6S, 10Wx9S, 14Wx3S, 14Wx4S, and 14Wx5S energy groups that alpha- and dense-particles in irradiated platelets became sparse in number or even disappeared, less electron density, irregularity in size and shape, and a tendency for these particles to ...
The in vivo pharmacological profile of SK&F 106760 [N alpha-acetyl-cyclo(S,S)-cysteinyl-N alpha-methylarginyl-glycyl-aspartyl-penicillamine-amide], a novel, potent glycoprotein IIb/IIIa (GPIIb/IIIa) antagonist has been investigated. In conscious dogs, SK&F 106760 (0.3-3 mg/kg i.v.) produced a dose-related inhibition of ex vivo whole blood platelet aggregation induced by collagen (5 micrograms/ml) with complete inhibition being produced for 5, 90 and 165 min after administration of 0.3, 1 and 3 mg/kg i.v., respectively. Plasma levels of SK&F 106760 were measured by high-performance liquid chromatography after i.v. bolus administration of 1 mg/kg. An initial alpha-disposition phase with a T1/2 of 11 +/- 6 min was followed by a longer terminal beta-elimination phase with a T1/2 of 66 +/- 12 min, which accounted for 79 +/- 9% of the total area under the plasma concentration-time curve. The apparent steady-state volume of distribution was 259 +/- 26 ml/kg and the plasma clearance was 3.4 +/- 0.8 ...
T3 were mainly composed by platelets and fibrin(ogen), while T6 were characterized by reduced platelet content, and increased leukocyte infiltration with appearance of undifferentiated progenitor cells. Differences between T3 and T6 were found in the cell cytoskeleton-associated proteome (beta-actin and tropomyosin 3 and 4). Using discovery proteomics, Pfn-1 was identified in the coronary thrombi at higher levels in T3 compared to T6. Plasma Pfn-1 levels were low in T3 patients, but increased in both coronary and peripheral circulation in T6 patients indicating release. In vitro platelet aggregation studies showed that platelets secrete Pfn-1 upon complete activation.. ...
The purpose of this project was to obtain some general knowledge of the platelet, and. to devise a quantitative means of analyzing two types of platelet aggregation curves: 1. the monophasic (rat platelet) curve, and 2. the biphasic (human platelet) curve. This was achieved. by the in vitro aggregation of platelets using various concentrations of epinephrine and noting the effect on the various parameters. It was found that increasing concentrations of epinephrine caused an inhibition of platelet aggregation in both the rat and the human ...
Many factors come into play when determining when and how frequent medical laboratory tests of any sort are made. The timing for laboratory tests rely on factors like the diagnosis, severity, diagnostic results, or completion of other procedures, tests, and treatments.. Lab tests may also be delayed when the condition is under specific phase of treatment or monitoring. Performing tests may also become necessary when certain signs or symptoms appear.. Due to changes in the bodys natural functioning throughout the course of the day, lab tests may be needed to be done at a certain time of the day.. Sometimes, it is necessary for you to prepare for a test by making changes on food or fluid intake. Lab tests may be timed in accordance to those changes. Also, the timing of tests may be based on increased and decreased levels in the amount of medications, drugs, or other substances taken in the body.. The age and gender of the person to undergo the test may also affect when and how often the lab test ...
Charles University Faculty of Pharmacy in Hradec Králové Department of Pharmacology & Toxicology Student: Nikola Kopková Supervisor: Assoc. Prof. Přemysl Mladěnka, Pharm.D., Ph.D. Title of diploma thesis: Antiplatelet effects of flavonoids The most common antioxidants in ordinary food are flavonoids. They show antioxidant and anti-aggregation effects and other positive effects on cardiovascular diseases. Flavonoids are promising candidates to be antiplatelet drugs. Although several mechanisms responsible for antiplatelet activity have been suggesteed, only a few have been documented by published studies. The inhibition of blood platelet aggregation by flavonoids is reversible, which is another important factor. Data on thrombin-induced aggregation are controversial, some claim that flavonoids have no effect, the others says they have positive effects. (In the case of quercetin and genistein, inhibition of aggregation induced by thrombin was documented). The effect on arachidonic acid in the
The aim of this study was to evaluate the effects of a fish oil preparation (MaxEPA) on hemostatic function and fasting lipid and glucose levels in non-insulin-dependent diabetic (NIDDM) subjects. Eighty NIDDM outpatients aged 55.9 yr (mean SD 11.5 yr) participated in a prospective double-blind placebo-controlled study of MaxEPA capsules (10 g/day) or olive oil (control) treatment over 6 wk. Patients received either MaxEPA or olive oil in addition to preexisting therapy. Metabolic and hemostatic variables were measured before treatment and after 3 and 6 wk. Platelet membrane eicosapentaenoic acid (EPA) content increased in the treatment group (P , 0.001). MaxEPA supplementation was associated with a significant fall in total triglycerides (P , 0.001) but did not affect total cholesterol (P = 0.7) compared with control treatment. Fasting plasma glucose increased after 3 wk (P = 0.01) but not after 6 wk (P = 0.17) treatment with MaxEPA. Spontaneous platelet aggregation in whole blood fell in the ...
Recent evidence suggests that endothelium-derived relaxing factor exhibits properties of nitric oxide. Like nitric oxide, it inhibits platelet function and mediates its effects by elevating intracellular cyclic GMP. In this study we have investigated the role of reduced thiol in the mechanism of action of endothelium-derived relaxing factor on platelets. Bovine aortic endothelial cells were grown on microcarrier beads and pretreated with aspirin before use. Endothelial cells stimulated with bradykinin or exposed to stirred medium expressed a dose-dependent inhibition of platelet aggregation that was potentiated by the reduced thiol, N-acetylcysteine. Endothelial cell-mediated platelet inhibition was attenuated by methylene blue. Inhibition of platelet aggregation by endothelial cells was associated with a rise in platelet intracellular cyclic GMP, an effect that was enhanced by N-acetylcysteine. These data show that 1) the reduced thiol N-acetylcysteine potentiates platelet inhibition by ...
TY - JOUR. T1 - Low concentration of oxidized low density lipoprotein suppresses platelet reactivity in vitro. T2 - An intracellular study. AU - Chou, Duen Suey. AU - Hsiao, George. AU - Shen, Ming Yi. AU - Fong, Tsorng Harn. AU - Lin, Chien Huang. AU - Chen, Tzeng-Fu. AU - Sheu, Joen Rong. PY - 2004/5. Y1 - 2004/5. N2 - The intracellular mechanisms underlying oxidized low density lipoprotein (oxLDL)-signaling pathways in platelets remain obscure and findings have been controversial. Therefore, we examined the influence of oxLDL in washed human platelets. In this study, oxLDL concentration-dependently (20-100 μg/mL) inhibited platelet aggregation in human platelets stimulated by collagen (1 μg/mL) and arachidonic acid (60 μM), but not by thrombin (0.02 U/mL). The activity of oxLDL was greater at 24 h in inhibiting platelet aggregation than at 12 h. At 24 h, oxLDL concentration-dependency inhibited intracellular Ca 2+ mobilization and thromboxane B2 formation in human platelets stimulated by ...
The Agg+ strain of S. sanguis induces platelet aggregation or clotting in vivo as predicted by the in vitro data. Aggregation in vitro is all-or-none with a dose-dependent delay (23). In vitro, rabbit platelets aggregate in response to the Agg+ strain in about two minutes. The experiments in vivo had been designed to record hemodynamic and cardiopulmonary responses upon a 1-min infusion of S. sanguis. Direct evidence for platelet aggregation or clotting in vivo include thrombocytopenia and, when compared to the Agg− strain, accumulation of 111Indium-labeled platelets in the lungs (Fig. 5), but not in the spleen. Platelets normally clear from the circulation to the spleen, but the 111Indium-labeled platelets used as tracers do not. The frequency and extent of manifestations of platelet clotting in vivo increase directly with the dose of inoculated Agg+S. sanguis.. Changes in heart rate and blood pressure occur more rapidly than would be predicted by the two minute lag time for in vitro platelet ...
The results of the present investigation demonstrate that insulin-stimulated platelets release sufficient amounts of ATP and/or adenosine to relax precontracted porcine coronary arteries. The signaling pathway initiated by insulin involves the activation of platelet eNOS, the soluble guanylyl cyclase and G kinase, and the association of VAMP-3 with the t-SNARE protein, syntaxin 2, and the release of adenine nucleotides and serotonin from dense granules. Since insulin-induced vasodilatation in vivo is sensitive to NOS inhibitors (8) but insulin does not acutely enhance NO production by endothelial cells (20), the NO-dependent release of platelet-derived vasodilator compounds may well account for the phenomenon of insulin-induced vasodilatation in vivo.. The effects of insulin on platelets is controversial since some studies have demonstrated that insulin attenuates thrombin-induced platelet aggregation (23-25), whereas others report that insulin may enhance platelet activation and aggregation ...
Staphylococcus aureus is an opportunistic pathogenic bacterium known for its ability to interact with platelets and modulate their function. S. aureus lipoproteins are one of the major groups of bacterial surface molecules and are released into the extracellular milieu where they are recognized by host immune cells. The aim of this study was to determine the role of S. aureus lipoproteins in S. aureus-platelet interactions. Platelet aggregation and binding assays using S. aureus wild type and lgt strains showed that, S. aureus lipoproteins contribute towards binding of the pathogen to platelets. Lipoproteins present in extracellular milieu also bind platelets. Platelet spreading, thrombus formation, agonist induced platelet aggregation and αIIbβ3 activation were inhibited by cell-free lipoproteins. CD36 was identified as the major platelet surface molecule interacting with S. aureus lipoproteins. Antibody neutralization demonstrated that functional inhibition of platelet activation caused by ...
Thromboregulation is the series of mechanisms in how a primary clot is regulated. These mechanisms include, competitive inhibition or negative feedback. It includes primary hemostasis, which is the process of how blood platelets adhere to the endothelium of an injured blood vessel. Platelet aggregation is fundamental to repair vascular damage and the initiation of the blood thrombus formation. The elimination of clots is also part of thromboregulation. Failure in platelet clot regulation may cause hemorrhage or thrombosis. Substances called thromboregulators control every part of these events. One primary function of thromboregulation is the control of primary hemostasis, which is the platelet aggregation process. Some thromboregulators enhance platelet aggregation and some others inhibit the process. Platelet aggregation plays a critical role in the genesis of a resulting thrombus. Adhesion should remain local, but platelet aggregation must grow exponentially to form a platelet thrombus and ...
T cell depletion with antithymocyte globulins (ATG) can be complicated by thrombopenia and. hypercoagulability. The underlying mechanism is still unclear. We found that binding of ATG to. platelets caused platelet aggregation, alpha-granule release, membrane phosphatidylserine exposure. and the rapid release of platelet microvesicles (MV). Platelet activation and MV release. were complement-dependent and required membrane insertion of C5b-8 but not stable lytic pore. formation by C5b-9. Full platelet aggregation and activation by ATG also required the low affinity. Fc gamma receptor FcγRII. MV release, however, was FcγRII-independent. Platelet MV. expressed high prothrombinase activity. Moreover, blocking C5 inhibited ATG-induced thrombin. generation in platelet rich plasma. In 19 hematopoietic stem cell and kidney transplant patients,. ATG treatment resulted in thrombopenia and increased plasma levels of d-dimer and thrombin-anti-. thrombin-complexes. Flow cytometric analysis of complement ...
This study enrolls the patients with PRU ≥208 who underwent coronary artery stent implantation and who are consistently treated with dual antiplatelet therapy
Platelets play a central role in maintaining biological hemostasis. Inappropriate platelet activation is responsible for thrombotic diseases such as myocardial infarction and stroke. Therefore, novel agents that can inhibit platelet activation are necessary. However, assays that monitor platelet aggregation are generally time-consuming and require high volumes of blood and specialized equipment. Therefore, a medium- to high-throughput assay that can monitor platelet aggregation would be considered useful. Such an assay should be sensitive, comparable to the gold standard assay of platelet aggregometry, and able to monitor multiple samples simultaneously but with low assay volumes. We have developed such a microtiter assay. It can assay an average of 60 independent treatments per 60 ml blood donation and demonstrates greater sensitivity than the current gold standard assay, namely platelet aggregation in stirring conditions in a platelet aggregometer. The microtiter plate (MTP) assay can detect ...
Platelets play a central role in maintaining biological hemostasis. Inappropriate platelet activation is responsible for thrombotic diseases such as myocardial infarction and stroke. Therefore, novel agents that can inhibit platelet activation are necessary. However, assays that monitor platelet aggregation are generally time-consuming and require high volumes of blood and specialized equipment. Therefore, a medium- to high-throughput assay that can monitor platelet aggregation would be considered useful. Such an assay should be sensitive, comparable to the gold standard assay of platelet aggregometry, and able to monitor multiple samples simultaneously but with low assay volumes. We have developed such a microtiter assay. It can assay an average of 60 independent treatments per 60 ml blood donation and demonstrates greater sensitivity than the current gold standard assay, namely platelet aggregation in stirring conditions in a platelet aggregometer. The microtiter plate (MTP) assay can detect ...
It has been reported that TGF-β1 plays an active role in platelet aggregation and the maintenance of integrin function (Hoying et al., 1999). Smad4 is a key molecule in the TGF-β family signaling pathway (Shi and Massague, 2003), and the effects of Smad4 on platelet function are unclear. Here, we observed that megakaryocyte/platelet-specific inactivation of Smad4 impaired the platelet aggregation induced by thrombin, ADP, and CRP as well as thrombus formation and hemostasis. The results from Fg binding (Fig. 3B), platelet aggregation (Fig. 2A), platelet spreading, and clot retraction studies (Fig. 3, C-F) revealed that lack of Smad4 results in defective platelet activation by affecting integrin αIIbβ3-mediated bidirectional signaling. The data shown in Figs. 4 and 5 indicated that the platelet functions regulated by Smad4 are mediated through the transcriptional regulation of key platelets signaling proteins, Syk, and ROCK2 in megakaryocytes.. The quantity of peripheral platelets is a ...
... stimulating activation of new platelets as well as increasing platelet aggregation. Platelet aggregation is achieved by ... Role of A2 in platelet aggregation[edit]. Thromboxane A2 (TXA2), produced by activated platelets, has prothrombotic properties ... Thromboxane is a vasoconstrictor and a potent hypertensive agent, and it facilitates platelet aggregation. ... there is a balance shift toward inhibition of vasoconstriction and platelet aggregation. It is believed that this shift in ...
Platelet aggregation. ↓Platelet adherence to vessel wall Novel. functions Antiinflammatory ↓IL-1, IL-6. ↑IL-10 ↓Proinflammatory ... Since thromboxane (an eicosanoid stimulator of platelet aggregation) is also downstream of COX enzymes, one might think that ... which inhibits platelet aggregation. PG-X, later known as prostacyclin, is 30 times more potent than any other then-known anti- ... so aspirin administration initially has little to no effect but eventually prevents platelet aggregation (the effect of ...
blood platelet aggregation; blood clotting; allergic reactions. NSAIDs inhibit its production to reduce incidence of strokes ... platelet aggregation, vascular smooth muscle contraction. PGI2 analogs used to treat vascular disorders like pulmonary ... vasodilation, inhibits platelets and pro-inflammatory cells. role(s) in human disease not yet proven[76][77] ... vasoconstriction, inhibits platelets. inactivating mutations in the 20-HETE-forming enzyme, CYP2U1, associated with Hereditary ...
"Pamicogrel inhibits platelet aggregation". Inpharma Weekly. 1272 (1): 11. January 2001. doi:10.2165/00128413-200112720-00021. ... Pamicogrel is a cyclooxygenase inhibitor that was under development for its anti-platelet-aggregation effects. Light P ( ...
A suspicion of congenital afibrinogenemia may appear on a platelet aggregation function test. The most common treatments are ... "Why Perform Platelet Aggregation?". Helena Biosciences. 2015 "Congenital afibrinogenemia". Retrieved 2015 ...
Platelet aggregation studies are optional. Serum protein electrophoresis results indicate evidence of a monoclonal spike but ... A low white blood cell count, and low platelet count in the blood may be observed. A low level of neutrophils (a specific type ... According to the model, factors predicting reduced survival are: Age > 65 years Hemoglobin ≤ 11.5 g/dL Platelet count ≤ 100×109 ... "Differential characteristics of Waldenström macroglobulinemia according to patterns of familial aggregation". Blood. 115 (22): ...
... moderate ethanol consumption on human platelet aggregation in platelet-rich plasma and whole blood". Alcoholism, Clinical and ... Alcohol decreases thrombosis (blood clotting). A. It reduces platelet aggregation. B. It reduces fibrinogen (a blood clotter). ...
... is a platelet aggregation inhibitor. It acts as a reversible cyclooxygenase inhibitor. The Merck Index (12th ed.). p ...
This promotes platelet adhesion and aggregation. Moreover, only once disruption of the plaque surface has occurred are these ...
... is a platelet aggregation inhibitor. It works as a thromboxane synthase inhibitor and a thromboxane receptor ...
... is a platelet aggregation inhibitor. Orefice G, Grasso A, Fazio N, Del Vecchio G, Volpe G, Coppola M, D'Alessio A, ...
In addition, PGE2 inhibits platelet aggregation. PGE2 also suppresses T cell receptor signaling and proliferation, and may play ...
Third, they connect to each other through receptor bridges: aggregation.[6] Formation of this platelet plug (primary hemostasis ... Therapy with platelets[edit]. Transfusion[edit]. Main article: Platelet transfusion. Indications[edit]. Platelet transfusion is ... Platelets also secrete platelet-derived growth factor (PDGF). Platelets modulate neutrophils by forming platelet-leukocyte ... Platelets secrete thromboxane A2, which acts on the platelet's own thromboxane receptors on the platelet surface (hence the so- ...
The result is inhibition of platelet aggregation. The US National Academy of Medicine updated Dietary Reference Intakes for ...
CO inhibits blood platelet aggregation and adhesion. CO may play a role as potential therapeutic agent. In mammals, carbon ... platelet aggregation, and leukocyte adhesion to the endothelium. Humans with atherosclerosis, diabetes, or hypertension often ...
It blocks thromboxane induced platelet aggregation and vasoconstriction. Waksman R, Gurbel P, Gaglia M (2014). Antiplatelet ...
10R,17S-diHDHA and to slightly lesser degrees 10R,17S-diHDHA and PDX inhibit the human platelet aggregation response to ... These E,Z,E PUFA are 20- to 100-fold stronger in inhibiting human platelet aggregation than two mono-hydroxyl-containing ... Croset M, Lagarde M (1983). "Stereospecific inhibition of PGH2-induced platelet aggregation by lipoxygenase products of ... potently inhibit blood platelet aggregation". FASEB Journal. 25 (1): 382-8. doi:10.1096/fj.10-161836. PMID 20833872. S2CID ...
Potent Inhibitors of the Aggregation of Human Platelets". Planta Medica. 51 (4): 300-3. doi:10.1055/s-2007-969496. PMID ...
... inhibits glucose transport and platelet aggregation. It blocks adenosine-induced apoptotic body formation ...
Platelet aggregation is another possible mechanism of injury. Blisters and spasm of blood vessels (vasospasm) can develop after ...
... a new class of anti-platelet drug. It functions by inhibiting thrombin-related platelet aggregation. This mechanism works by a ... Unlike many other medication, vorapaxar does not affect ADP-mediated platelet aggregation, coagulation parameters, or bleeding ... Vorapaxar is a new anti-platelet drug that is part of the PAR-1 antagonist family, ... different pathway than other anti-platelet medications such as aspirin and P2Y12 inhibitors. ...
Antiplatelets are drugs that interfere with platelet aggregation. These drugs are prescribed in certain medical conditions/ ... At the time of extraction a platelet rich fibrin (PRF) membrane containing bone growth enhancing elements is placed in the ... Peck MT, Marnewick J, Stephen L (2011). "Alveolar ridge preservation using leukocyte and platelet-rich fibrin: a report of a ... Khiste SV, Naik Tari R (2013). "Platelet-Rich Fibrin as a Biofuel for Tissue Regeneration". ISRN Biomaterials. 2013: 1-6. doi: ...
"Acute microvascular platelet aggregation after subarachnoid hemorrhage (SAH)." J Neurosurg 2005. 102(6) 1094- 1100. PMID ...
Uraemia can lead to alteration of platelet aggregation. This situation, combined with the use of heparin and other ... Aspirin is characterized by an anti-platelet activity and thus its use should be avoided in uremic patients. The challenge in ...
PDE3 is an important player in platelet aggregation. It has been reported that higher concentration of cGMP causes inhibition ... Interplay between those two functions seems to mediate an opposing regulation of cAMP in platelets. PDE2 regulates cardiac L- ... PDE2 is expressed in various tissues, for example: adrenal medulla, brain, heart, platelet, macrophages and endothelial cells. ... that PDE2 might play an important role in the regulation of elevated intracellular concentrations of cAMP and cGMP in platelets ...
PDE3 is an important player in platelet aggregation. It has been reported that higher concentration of cGMP causes inhibition ... Interplay between those two functions seems to mediate an opposing regulation of cAMP in platelets (See review article [3]).. ... PDE2 is expressed in various tissues, for example: adrenal medulla, brain, heart, platelet, macrophages and endothelial cells. ... intracellular concentrations of cAMP in cardiomyocytes and of cAMP and cGMP in platelets ...
... signaling may contribute to platelet activation and aggregation. A PKA/PKG phosphorylation site has been identified in ... Zimman A, Titz B, Komisopoulou E, Biswas S, Graeber TG, Podrez EA (2014). "Phosphoproteomic analysis of platelets activated by ... Significantly increased phosphorylation on S249 of CASS4, also in the unstructured domain, after platelet stimulation with the ... which may implicate CASS4 mediated signaling in platelet hyperreactivity. There are currently no therapeutic approaches ...
... also inhibits platelet aggregation and smooth muscle proliferation. The pharmacokinetics of continuous ... Because of treprostinil's inhibiting effect on platelet aggregation, there is an increased risk of bleeding, especially among ... which inhibited platelet aggregation. PG-X, which later would become known as prostacyclin, was 30 times more potent than any ... isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet aggregation". ...
Furthermore, it is known that nicergoline inhibits platelet aggregation. Studies have shown that nicergoline also increases ... Migraines of vascular origin Coadjutant therapy in clinical situations accompanied by platelet hyper-aggregability, arterial ...
Platelet adhesiveness. Other. *Erythrocyte aggregation. Retrieved from " ...
aggregation *Glanzmann's thrombasthenia. *platelet storage pool deficiency *Hermansky-Pudlak syndrome. *Gray platelet syndrome ... A low platelet count and positivity for antibodies against β2-glycoprotein 1 or phosphatidylserine may also be observed in a ... Often, this disease is treated by giving aspirin to inhibit platelet activation, and/or warfarin as an anticoagulant. The goal ... Other common findings, although not part of the APS classification criteria, are low platelet count, heart valve disease, and ...
Ross CA, Poirier MA (July 2004). "Protein aggregation and neurodegenerative disease". Nat. Med. 10 Suppl (7): S10-7. doi: ... platelets, and monocytes. T cell activation is accompanied by a strong up-regulation of PrP, though it is not requisite. The ...
"Phospholipase D activity facilitates Ca2+-induced aggregation and fusion of complex liposomes". Am. J. Physiol. 272 (4 Pt 1): ...
Binding of antigens to IgE already bound by the FcεRI on mast cells causes cross-linking of the bound IgE and the aggregation ... Fc receptors are also found on eosinophils, monocytes, macrophages and platelets in humans. There are two types of Fcε ...
The P-selectin then promotes platelet aggregation through platelet-fibrin and platelet-platelet binding. ... platelet alpha granule membrane. • platelet dense granule membrane. • external side of plasma membrane. • extracellular space. ... P-selectin is also very important in the recruitment and aggregation of platelets at areas of vascular injury. In quiescent ... platelet degranulation. • regulation of integrin activation. • cell adhesion. • defense response to Gram-negative bacterium. • ...
Expression of anger has been strongly associated with chronically elevated blood pressure and with the aggregation of platelets ...
Also there is not as much inhibition of aggregation of platelets. In this case, the greater aggregation of platelets produce ... and reduce aggregation of platelets. Aggregating platelets stimulate ADP to act on endothelial cells and help them induce ... However, aggregating platelets also stimulate thromboxane A2 and serotonin which can induce contraction of the smooth muscle ...
... can cause unpredictable serious and life-threatening blood and cardiovascular reactions including low platelet count ... which facilitates the aggregation of cytotoxic heme. Free cytotoxic heme accumulates in the parasites, causing their deaths.[31 ... low blood platelets, and an irregular heartbeat.[2] Use can make one more prone to sunburn.[2] While it is unclear if use ...
EPA and DHA supplementation has been shown to reduce blood platelet aggregation in vegetarians, but a direct link to ... Normalization of Hyperhomocysteinemia with Vitamin B12 and Reduction of Platelet Aggregation with n-3 Fatty Acids". Thrombosis ...
... discovered that an extract from tomato had a positive effect in the prevention of blood platelet aggregation.[4][5][6] ... Duttaroy, Asim K. (June 2018). Human Blood Platelet Function: Applications in Cardiovascular Health. Wiley. pp. 1-300. ISBN 978 ... "Effects of antiplatelet components of tomato extract on platelet function in vitro and ex vivo: A time-course cannulation ...
Ristocetin-induced platelet aggregation. .mw-parser-output .nobold{font-weight:normal}. clotting factors:. *Prothrombin time ...
First, zinc-containing metalloproteases act upon capillary endothelial cells to cause platelet aggregation and hemorrhage.[14] ... Chang, Mei-Chi (1998). "Antithormbotic Effect of Crotalin, a Platelet Membrane Glycoprotein Ib Antagonist From Venom of ... blocking aggregation.[15] These two starkly different effects may seem counterproductive, but the effect should be profound. ... Second, the platelet antagonist crotalin creates a severe bleeding effect as it binds to the surface proteins, ...
Platelet aggregation inhibitor[2]. clopidogrel, ticagrelor -axine. Dopamine and serotonin-norepinephrine reuptake inhibitor[2] ...
Coagulation (Fibrinolysis) · Clot retraction · Platelet adhesiveness. Other. Erythrocyte aggregation. සැකිල්ල:Myeloid navs ...
F. necrophorum produces hemagglutinin which causes platelet aggregation that can lead to diffuse intravascular coagulation and ... Platelet count can be low or high. Liver and kidney function tests are often abnormal. ...
Eff ect of policosanol on platelet aggregation and serum levels of arachidonic acid metabolites in healthy volunteers. ... Eff ect of policosanol on platelet aggregation in healthy volunteers. Intern. J. Clin. Pharmacol. Res. 1996. ... Eff ect of policosanol succesive dose increase in platelet aggregation healthy volunteers. Pharmacol. Res. 1995. ...
... inhibits blood platelet aggregation and adhesion, suppresses, reverses, and repairs the damage caused by inflammatory responses ...
The possible exceptions may be aspirin and naproxen due to their anti-platelet aggregation properties. ...
... producing an inhibitory effect on platelet aggregation during the lifetime of the affected platelet (8-9 days). This ... Thromboxanes are responsible for the aggregation of platelets that form blood clots. Heart attacks are caused primarily by ... Since platelets have no DNA, they are unable to synthesize new PTGS once aspirin has irreversibly inhibited the enzyme, an ... For some people, aspirin does not have as strong an effect on platelets as for others, an effect known as aspirin-resistance or ...
Platelet function. adhesion (Bernard-Soulier syndrome) · aggregation (Glanzmann's thrombasthenia) · platelet storage pool ...
... which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi. ...
Beyond this, HRT improves heart contraction, coronary blood flow, sugar metabolism, and decreases platelet aggregation and ...
The solvent creates an environment in which the aggregation reaction between the lipid coat and the detergent happen more ... de Cock, et al.,"The Mirasol Evaluation Program: Use of Mirasol PRT for Platelets in Routine Clinical Practice," Transfusion ... Ruane PH, et al., "Photochemical Inactivation of Selected Viruses and Bacteria in Platelet Concentrates Using Riboflavin and ...
... which happens after the initial platelet aggregation and ultimately leads to formation of fibrin and stable aggregated platelet ... Batroxobin, a toxin from a snake venom, clots platelet-rich plasma without affecting platelet functions (lyses fibrinogen). ... antiplatelet drugs inhibit platelet aggregation (clumping together), whereas anticoagulants inhibit specific pathways of the ... and its mixed prescription on the high molecular weight dextran-induced blood stasis in rats and human platelet aggregation". ...
2001). "Activation of protease-activated receptors by gingipains from Porphyromonas gingivalis leads to platelet aggregation: a ... ೧೯೮೭). "Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death". ...
... thus stimulating platelet and monocyte aggregation around the xenotransplanted organ, causing severe clotting.[32] Additionally ... Complement activation causes a cascade of events leading to: destruction of endothelial cells, platelet degranulation, ... and platelets. The response is characterized by an inflammatory infiltrate of mostly macrophages and natural killer cells (with ... spontaneous platelet accumulation may be caused by contact with pig von Willebrand factor.[32] ...
... and keep the blood from clotting by excreting an anticoagulant or platelet aggregation inhibitor.[45][46] ... Common Origins for Blood Coagulation and Platelet Aggregation Inhibitors from Soft Ticks of the Genus Ornithodoros". Molecular ...
... platelet aggregation inhibitor (CHEBI:50427). δ-guaiene (CHEBI:63447) has role platelet aggregation inhibitor (CHEBI:50427). (E ... platelet aggregation inhibitor (CHEBI:50427). (S)-glaucine (CHEBI:5373) has role platelet aggregation inhibitor (CHEBI:50427). ... platelet aggregation inhibitor (CHEBI:50427). S-nitroso-L-cysteine (CHEBI:138935) has role platelet aggregation inhibitor ( ... platelet aggregation inhibitor (CHEBI:50427). benzo[d]isothiazol-3-one (CHEBI:167099) has role platelet aggregation inhibitor ( ...
The platelet aggregation blood test checks how well platelets, a part of blood, clump together and cause blood to clot. ... Platelet aggregation - blood; platelet aggregation, hypercoagulable state - blood. In: Chernecky CC, Berger BJ, eds. Laboratory ... The platelet aggregation blood test checks how well platelets, a part of blood, clump together and cause blood to clot. ... Your provider may order this test if you have signs of a bleeding disorder or a low platelet count. It may also be ordered if a ...
Patients whole blood platelet count must be ,112,500/cu mm (add-on complete blood count (CBC, CPT 85027) and clot retraction ... Platelet Aggregation. Platelet aggregation Core Lab, Coagulation. Battery Members. Agonists include ADP, Arachidonic Acid, ...
The platelet aggregation blood test checks how well platelets, a part of blood, clump together and cause blood to clot. Learn ... Platelet aggregation - blood; platelet aggregation, hypercoagulable state - blood. In: Chernecky CC, Berger BJ, eds. Laboratory ... The platelet aggregation blood test checks how well platelets. , a part of blood, clump together and cause blood to clot. ... platelet count. . It may also be ordered if a member of your family is known to have a bleeding disorder due to platelet ...
... ,ARUP Laboratories is a national reference laboratory and a worldwide leader in innovative ... Platelet Incubator TPSRI-16. 4. Platelet Incubator 3603. 5. Platelet Incubator 3606. 6. Platelet Incubator 3609. 7. i. Series ... Platelet Incubator 3612. 9. i. Series Floor Model Platelet Incubator PC4200i. 10. i. Series Floor Model Platelet Incubator ...
Platelet testing and research company Aggredyne, Inc. has received U.S. Food and Drug Administration (FDA) clearance for ... ... Aggredyne receives FDA clearance for ADP platelet aggregation testing cartridge. News provided by ... instrument and associated assays for testing platelet aggregation in the individual patients. The companys patented products ... The company is also developing additional assays to be used with its instrument(s) in the anti-platelet therapy field as well ...
The reference range is a normal biphasic pattern of aggregation in response to specific platelet activators (see image below).{ ... Platelet Aggregation) and Platelet Aggregation What to Read Next on Medscape. Related Conditions and Diseases. * Platelet ... Platelet aggregation studies test the clumping response of platelets to various platelet activators (eg, ADP, collagen, ... Platelet secretion defects can provide greater diagnostic sensitivity than platelet aggregation testing alone. [1, 2, 3] ...
The present invention relates to methods for regulating platelet adhesion and aggregation in a subject. The methods involve ... 0091] TSP-1 is a major component of platelet α-granules which is secreted upon platelet activation and aggregation. TSP-1 was ... 2. A method for reducing platelet adhesion and aggregation in a subject, the method comprising administering to the subject an ... 4. A method for reducing platelet adhesion and aggregation in a subject, the method comprising administering to the subject a ...
The Platelet Aggregation Tests. Human platelet suspensions were prepared as previously described [27]. In this study, human ... Each person had his/her own 0% PRP and 100% PPP aggregation calibration. Before aggregation was started, standard platelet ... The Inhibition Effect of Different Components on Platelet Aggregation Induced by Different Agonists. Results of the platelet ... and the most antiplatelet aggregation effect occurred in the collagen-included platelet aggregation test group with an ...
The ristocetin-induced platelet aggregation (RIPA) is an ex vivo assay for live platelet function. It measures platelet ... it causes agglutination of fixed platelets or initiates the initial agglutination phase of aggregation of live platelets. The ... Ristocetin cofactor assay uses the patients platelet poor plasma (with vWF but no platelets) and adds ristocetin and exogenous ... results of the ristocetin-induced platelet aggregation in some characteristic diseases are the following: Type 1 vWD: ...
AGE inhibits platelet aggregation by increasing cyclic nucleotides and inhibiting fibrinogen binding and platelet shape change. ... Pharmacological Actions : Platelet Aggregation Inhibitors. Additional Keywords : Aspirin-Vitamin b12 Deficiency, Drug-Nutrient ... Pharmacological Actions : Platelet Aggregation Inhibitors. Additional Keywords : Natural Substances Versus Drugs, Phytotherapy ... 45 Abstracts with Platelet Aggregation Inhibitors Research. Filter by Study Type. Animal Study. ...
Fill in any or all of the fields below. Click on the label to the left of each search field for more information or read the Help ...
A platelet is a blood cell that helps your blood to clot. This test is scheduled with the lab through the Bleeding Disorders ... Platelet aggregation is a blood test that measures how well the platelets stick to one another. ... Platelet aggregation is a blood test that measures how well the platelets stick to one another. A platelet is a blood cell that ...
We employed whole blood platelet aggregation analysis based on impedance as well as determination of ATP release from platelet ... Whole Blood Platelet Aggregation and Release Reaction Testing in Uremic Patients. Jay Zeck,1 Jason Schallheim,1 Susie Q. Lew,2 ... ATP release had a low response to arachidonic acid (0.37 ± 0.26 nmoles, reference range: 0.6-1.4 nmoles). Platelet aggregation ... Platelet function analysis utilizing platelet-rich plasma and optical density based aggregometry fails to identify patients at ...
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canadas national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc. ...
HIPAA stands for Heparin-Induced Platelet Aggregation Assay. HIPAA is defined as Heparin-Induced Platelet Aggregation Assay ... How is Heparin-Induced Platelet Aggregation Assay abbreviated? ... Induced-Platelet-Aggregation-Assay-(HIPAA).html. *APA style: ... Induced-Platelet-Aggregation-Assay-(HIPAA).html,HIPAA,/a,. ... Induced-Platelet-Aggregation-Assay-(HIPAA).html. *Chicago style ... n.d.) Acronym Finder. (2019). Retrieved July 21 2019 from ...
... or to a once-washed platelet suspension causes platelet aggregation. This aggregation is associated with phagocytosis of the ... from the platelets. Adenosine and adenosine monophosphate, which are known to inhibit platelet aggregation induced by ADP, also ... PLATELET PHAGOCYTOSIS AND AGGREGATION. Henry Z. Movat, William J. Weiser, Michael F. Glynn, James F. Mustard ... blocks platelet aggregation and phagocytosis. This is also true for the chelating agent ethylenediaminetetraacetate (EDTA). ...
Platelet Aggregation Devices Market Report Categories the Global Market by Application (Diagnostic, Research, Orthopedic, CVD, ... Figure 27 Platelet Aggregation Systems to Contribute the Maximum to the Platelet Aggregation Products Market Growth in the U.S ... Table 16 Global Platelet Aggregation Devices Market Size, By End User, 2013 2020 (USD Million). Table 17 Platelet Aggregation ... 4.2 Global Platelet Aggregation Devices Market, By Region (2015 2020) 4.3 Platelet Aggregation Devices Market, By Product (2015 ...
... inhibition of platelet aggregation ex vivo, and intra-platelet cAMP levels. Basal U46619 and ADP -induced platelet aggregation ... Inhibition of platelet aggregation ex vivo is repressed in apolipoprotein E deficient mice.. Carrier É1, Houde M1, Grandbois M1 ... Intravenous infusion of PGI2 also failed to inhibit platelet aggregation ex vivo in 18- to 20-week-old ApoE-/- mice. ... Systemically administered endothelin-1 (ET-1) or bradykinin (BK) inhibited platelet aggregation in a similar fashion in 8- to ...
... Study ID. STU 082012-089 ... Participants with also be asked to not eat foods known to affect platelet function (coffee, chocolate, grapes, and alcohol) 48 ... known to affect platelet function will be assessed and patients on those will be asked to discontinue these. ... platelet factor 4, beta thromboglobulin and VWF antigen levels and activity). Participants will be administered aspirin 81 mg ...
Percent inhibition of maximum extent and rate of aggregation of 5 µM ADP-induced platelet aggregation. ... Platelet Aggregation Inhibition in Children on Clopidogrel (PICOLO). The safety and scientific validity of this study is the ... Platelet Aggregation Inhibitors. Purinergic P2Y Receptor Antagonists. Purinergic P2 Receptor Antagonists. Purinergic ... Dose-Ranging Pharmacodynamic Assessment of Platelet Aggregation Inhibition With Clopidogrel in Children of Blalock-Taussig ...
In the present study, the process of platelet aggregation is considered. In blood flow near the entry to an aneurysm, red blood ... Keywords: computational fluid dynamics, platelet aggregation, aneurysm. 1 Introduction Rupture of a cerebral artery aneurysm ... The ensuing release of adenosine diphosphate (ADP) induces the aggregation. Making reference to actual aggregation curves of ... the authors have modelled the rate at which the density of aggregated platelets continues to increase in the aggregation ...
Platelet aggregation [ Time Frame: 2 hours ]. Platelet aggregation is measured by means of Multiple Electrode Aggregometry (MEA ... Platelet Aggregation During the Shift From Clopidogrel to Ticagrelor (SHIFT-OVER). The safety and scientific validity of this ... Platelet Aggregation During Pharmacological Shift From Clopidogrel to Ticagrelor in Patients With Acute Coronary Syndrome. ... Platelet Aggregation Inhibitors. Purinergic P2Y Receptor Antagonists. Purinergic P2 Receptor Antagonists. Purinergic ...
Finally, Exisulind reduced platelet aggregation, which was mediated via PKG activation. This study demonstrated that Exisulind ... We examined the effects of PKG activation by Exisulind on neointimal formation, platelet aggregation, and re-endothelialization ... inhibits neointimal formation and platelet aggregation while increasing re-endothelialization via PKG pathway. These findings ... Inhibition of platelet aggregation by Exisulind.. (A) Platelet aggregometer with platelet rich-plasma from a healthy donor ...
PubMed journal article Postprandial platelet aggregation: effects of different meals and glycemic inde were found in PRIME ... Postprandial Platelet Aggregation: Effects of Different Meals and Glycemic Index. Eur J Clin Nutr. 2012;66(6):722-6. PubMed ... Postprandial platelet aggregation: effects of different meals and glycemic index.. Eur J Clin Nutr 2012; 66(6):722-6EJ ... "Postprandial Platelet Aggregation: Effects of Different Meals and Glycemic Index." European Journal of Clinical Nutrition, vol ...
... 04.04.2006 ... in human platelets, more specifically of MRP4.. Further Information: PDF PVA Mecklenburg-Vorpommern AG. Phone: +49 (0)381/49 74 ...
O. Odugbesan, K.J.C Dallinger, A.H. Barnett; Influence of Diabetic Control on Platelet Aggregation. Clin Sci (Lond) 1 December ...
... The purpose of this study is to determine whether shear-induced platelet aggregation is able to discriminate ... Platelet aggregation and leucocyte activation seem to be involved in the pathogenesis. The aim of our study is to compare SIPA ... More From BioPortfolio on "Pilot Study on Shear-induced Platelet Aggregation in Acute Coronary Syndromes". *Related Companies* ... The purpose of this study is to determine whether shear-induced platelet aggregation is able to discriminate first acute ...
What is Platelet aggregation inhibitor? Meaning of Platelet aggregation inhibitor medical term. What does Platelet aggregation ... Looking for online definition of Platelet aggregation inhibitor in the Medical Dictionary? Platelet aggregation inhibitor ... redirected from Platelet aggregation inhibitor) Antiplatelet drug. Drug that inhibits platelets from aggregating to form a plug ... Platelet aggregation inhibitor , definition of Platelet aggregation inhibitor by Medical dictionary https://medical-dictionary. ...
b) PGE2 (10-4 M) induced aggregation of IP-deficient platelets. The failure to observe aggregation of platelets deficient in ... alone has no effect on platelet aggregation ex vivo, this lipid mediator can stimulate or inhibit platelet aggregation ... alone is sufficient to induce aggregation of IP-deficient platelets, but not wild-type platelets. Further aggregation observed ... The dual effect of PGE2 on platelet aggregation. (a) Wild-type platelets are exposed to a low concentration of U46619 (1 μM), ...
  • Platelet inhibition has shown improved short- and long-term clinical outcomes for CVD patients. (
  • Inhibition of platelet aggregation ex vivo is repressed in apolipoprotein E deficient mice. (
  • Apolipoprotein E deficient mice (ApoE-/-), a mouse model of atherosclerosis, and their wild-type (WT) counterparts were used to assess agonist-stimulated synthesis of prostacyclin (PGI 2 ), inhibition of platelet aggregation ex vivo, and intra-platelet cAMP levels. (
  • PICOLO is a double blind placebo controlled phase II dose ranging, dose escalating study in patients of Blalock-Taussig age categories (neonates and infants/toddlers), to determine the dose providing inhibition of platelet aggregation similar to adults. (
  • Dosing of clopidogrel for platelet inhibition in infants and young children: primary results of the Platelet Inhibition in Children On cLOpidogrel (PICOLO) trial. (
  • However it is unknown whether a loading dose is needed to maintain a satisfactory inhibition of platelet aggregation in patients who are already treated with a previous generation P2Y12 inhibitor (clopidogrel) during the passage to the newer compound ticagrelor. (
  • Interestingly, PKG is present at high levels in platelets and associated with inhibition of platelet aggregation 16 . (
  • Poor inhibition of platelet aggregation by anti-platelet agents predicts future cardiovascular events. (
  • and 3) compare inhibition of platelet aggregation from baseline after 2 weeks of aspirin therapy and another 2 weeks of clopidogrel therapy added to aspirin in Chronic Kidney Disease vs. non-Chronic Kidney Disease patients. (
  • Inhibition of platelet aggregation, compared to the control lacking active enzyme, suggests the formation of the thienopyridine active metabolite and its reaction with the platelet P2Y12 receptor. (
  • No inhibition of platelet aggregation was observed in this system when thrombin was used as the agonist. (
  • Of the CYP's tested, CYP3A4, CYP2B6 and CYP2C19 showed increasing inhibition of platelet aggregation with time in this system while CYP1A2, CYP2D6 and CYP2C9 did not. (
  • Increasing the concentration of CYP3A4 and CYP2B6 from 20 nM to 80 nM allowed for complete inhibition of platelet aggregation to be achieved over the 20 minute time course of the experiment. (
  • Pharmacologic inhibition of TREM-1 reduces platelet activation as well as platelet aggregation induced by collagen, ADP, and thrombin in human platelets. (
  • Results of the FABOLUS-FASTER trial offer clinicians further insight into the effects of cangrelor, tirofiban, and chewed or integral prasugrel for immediate inhibition of platelet aggregation. (
  • Results of the FABOLUS-FASTER trial indicate tirofiban may be more effective than cangrelor in reducing risk of acute ischemic complications when used for bridging platelet inhibition in heart attack patients undergoing percutaneous coronary intervention (PCI). (
  • Presented as part of PCR e-course due to the cancellation of EuroPCR 2020, results of the FABOLUS-FASTER trial, which examined the pharmacodynamic effects of cangrelor and tirofiban as well as chewed and integral prasugrel, support the use of parenteral drugs for achieving immediate inhibition of platelet aggregation (IPA) and bridging the inhibition gap often seen with oral P2Y12 inhibitors. (
  • Nonsteroidal antiinflammatory drugs such as diclofenac or naproxen may interfere with the inhibition of platelet aggregation by aspirin, because they all interact with the platelet cycloox. (
  • Inhibition of phosphoinositide 3-kinase (PI3-kinase) has been shown to cause platelet disaggregation. (
  • These platelets did not release NO, and PI3-kinase inhibition led to decreased superoxide but not platelet disaggregation. (
  • The effects of NO, a well-established regulator of platelet function, are similar to the effects of PI3-kinase inhibition. (
  • Inhibition of PI3-kinase and the addition of exogenous NO donors appear to have additive platelet inhibitory effects, 8 however, the relevance of these findings to endogenous NO release is unclear. (
  • Acetylcholine and to a lesser extent nicotine show potential for therapeutic inhibition of mCRP-induced inflammation and cell and platelet adhesion. (
  • Gremmel T, Yanachkov IB, Yanachkova MI, Wright GE, Wider J, Undyala VV, Michelson AD, Frelinger AL, Przyklenk K. Synergistic Inhibition of Both P2Y1 and P2Y12 Adenosine Diphosphate Receptors As Novel Approach to Rapidly Attenuate Platelet-Mediated Thrombosis. (
  • The experiments describe the inhibition of platelet aggregation in vitro and the diminished accretion of the artificial thrombus in the Chandler apparatus by 2-bromolysergic acid diethylamide (BOL-148), imipramine, chiorpromazine, diphenhydramine, atropine, l -hyoscyamine and homatropine. (
  • Thrombin aggregation was more susceptible to inhibition than ADP aggregation but less susceptible than 5-HT-induced clumping. (
  • These results correlate well with the inhibition of serotonin uptake into platelets by these drugs. (
  • Therefore, NADPH has a platelet aggregation inhibition function and can be used as a potential platelet aggregation inhibitor. (
  • Application of adenylate kinase to inhibition of the aggregation and to the deaggregation of blood platelets. (
  • In this context, inhibition of the platelet function (adhesion/aggregation) could contribute to the prevention of atherothrombosis, the leading cause of cardiovascular morbidity. (
  • Inhibition of platelet aggregation by carbon monoxide is mediated by activation of guanylate cyclase. (
  • It is concluded that cGMP is an important feedback regulator of the Pl response and that already a 25% increase in its steady state levels can cause inhibition of platelet aggregation. (
  • 11 Platelet stimulation by strong agonist is mediated by additional or distinct intracellular events compared with stimulation by weak agonists, 11-13 suggesting that the inhibition of one of these pathways may not necessarily inhibit platelet aggregation as observed clinically. (
  • Potentiation of clopidogrel active metabolite formation by rifampicin leads to greater P2Y12 receptor blockade and inhibition of platelet aggregation after clopidogrel. (
  • Use of prasugrel in PCI patients would result in greater inhibition of platelet aggregation (IPA) than high-dose clopidogrel, both during the loading and maintenance phases. (
  • The main secondary endpoints for the LD and MD phases were mean MPA with 20 µmol/L ADP, VASP platelet reactivity index, and mean VerifyNow P2Y 12 assay percent inhibition. (
  • In addition, prasugrel demonstrated significantly greater antiplatelet effects compared with clopidogrel, as assessed by various secondary endpoints over the same time points such as: 1) significantly higher levels of IPA with 5 µmol/L ADP, 2) lower levels of maximal platelet aggregation (MPA) with 5 and 20 µmol/L ADP, 3) higher vasodilator-stimulated phosphoprotein (VASP) platelet reactivity index, and 4) greater percent inhibition with the VerifyNow P2Y 12 assay. (
  • Almaghrabi, SY 2017 , 'Inhibition of platelet aggregation by vanilloid-like agents: investigation of possible mechanisms', PhD thesis, University of Tasmania. (
  • The aims of the investigations described in Chapter 2 were to firstly to confirm TRPV1 expression on human platelets, and then to determine whether vanilloid inhibition of in vitro platelet aggregation was receptor mediated, i.e., through TRPV1 channels, and/or CB1 or CB2 receptors. (
  • Further studies showed that 5-HT2 receptors and effects on platelet secretion are not involved in PCP-mediated inhibition of epinephrine-induced platelet aggregation. (
  • Luzak B, Golanski J, Rozalski M, Krajewska U, Olas B, Watala C. Basic researchExtract from Aronia melanocarpa fruits potentiates the inhibition of platelet aggregation in the presence of endothelial cells. (
  • There are no literature reports on the modulation of endothelial cell (EC)-induced inhibition of platelet aggregation by polyphenolic compounds. (
  • The present invention relates to methods for regulating platelet adhesion and aggregation in a subject. (
  • 2. A method for reducing platelet adhesion and aggregation in a subject, the method comprising administering to the subject an effective amount of TSP-1 or a functional fragment thereof. (
  • 4. A method for reducing platelet adhesion and aggregation in a subject, the method comprising administering to the subject a nucleic acid molecule comprising a sequence encoding TSP-1 or a functional fragment thereof. (
  • 9. A method for promoting platelet adhesion and aggregation in a subject, the method comprising administering to the subject an antagonist of TSP-1. (
  • Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. (
  • 9 Superoxide generated by stimulated platelets can increase both platelet adhesion and aggregation, 9 presumably as a consequence of its reaction with NO and the attenuation of NO bioactivity. (
  • We have searched, identified and structurally characterized novel snake venom proteins that modulate platelet adhesion and aggregation by interacting with vWF.a) We screened. (
  • The PFA-100 TM constitutes a recently developed platelet function analyzer, which measures primary hemostasis in vitro by simulating in vivo platelet adhesion and aggregation under high shear stress [ 9 ]. (
  • Platelets aggregation was induced by different agonists including adenosine diphosphate (ADP, 10 μ M), thrombin receptor activator peptide (TRAP, 50 μ M), and collagen (5 μ g/mL). (
  • This aggregation is associated with phagocytosis of the latex particles by the platelets and appears to be due to release of adenosine diphosphate (ADP) from the platelets. (
  • The ensuing release of adenosine diphosphate (ADP) induces the aggregation. (
  • Maximum aggregation in response to adenosine diphosphate (ADP) decreased after saline-based HES infusion, but not after balanced solution-based HES infusion. (
  • Methods and Results- Aggregation, measured using a platelet-counting technique, occurred in response to ATP and was maximal at 10 to 100 μmol/L. It was abolished by MRS2179, AR-C69931, and creatine phosphate/creatine phosphokinase, implying that conversion to adenosine diphosphate (ADP) is required. (
  • Large quantities of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) are present in erythrocytes, platelets, and other cells and tissues and can leave the cells via physical damage or exocytosis. (
  • The present study evaluated the effect of T. sarmentosa on adenosine diphosphate-induced platelet aggregation. (
  • Our results showed that aqueous stem extract of T. sarmentosa inhibited adenosine diphosphate-induced platelet aggregation. (
  • In addition, we found components in T. sarmentosa, including caffeic acid, rosmarinic acid, salvianolic acid, play important roles in mediating adenosine diphosphate-induced platelet aggregation suppression. (
  • Furthermore, treatment of platelets with T. sarmentosa , or the components in stem extract of T. sarmentosa , suppressed adenosine diphosphate-induced release of thromboxane A2 and arachidonic acid and surface PAC-1 expression. (
  • New highly active antiplatelet agents with dual specificity for platelet P2Y1 and P2Y12 adenosine diphosphate receptors. (
  • 5-Hydroxytryptamine (5-HT) and adenosine diphosphate (ADP) caused platelet aggregation in sheep platelet-rich plasma in concentrations of 1.2 and 1.3 µM, as did thrombin (0.2 U/ml). (
  • Platelets from T. cruzi -infected mice were 2-6-fold more sensitive to aggregation induced by adenosine diphosphate and sodium arachidonate than controls. (
  • To develop novel anti-ischemic stroke agents with better therapeutic efficacy and bioavailability, we designed and synthesized a series of 3-alkyl-2,3-dihydro-1H-isoindol-1-ones compounds (3a-i) derivatives, one of which (3d) exhibited the strongest inhibitory activity for the adenosine diphosphate-induced and arachidonic acid-induced platelet aggregation. (
  • SEVERAL studies of the effects of inhalation anesthetic agents on platelet function have been reported since Ueda 1 demonstrated in 1971 that clinical concentrations of halothane inhibited adenosine diphosphate (ADP)-induced platelet aggregation. (
  • Results On arising and standing, platelet aggregation increased by 71% (p ≤ 0.01) and 27% (p ≤ 0.03) in response to collagen and adenosine diphosphate, respectively. (
  • 0.05) increase in platelet aggregation in response to adenosine diphosphate. (
  • Furthermore, the inhibitory effects of vanilloids on in vitro platelet aggregation induced by collagen, Adenosine diphosphate (ADP) and arachidonic acid (AA) were found not to be TRPV1-, CB1- or CB2- receptor mediated. (
  • Platelet storage pool deficiency is a type of coagulopathy characterized by defects in the granules in platelets, particularly a lack of granular non-metabolic adenosine diphosphate. (
  • Individuals with adenosine diphosphate deficient storage pool disease present a prolonged bleeding time due to impaired aggregation response to fibrillar collagen. (
  • An increased aggregation response to low-dose ristocetin (a type IIb von Willebrand disease-like defect) is associated with thrombus formation. (
  • is a platelet aggregation inhibitor mainly used during and after coronary artery procedures such as angioplasty to prevent platelets from sticking together and causing thrombus formation within the coronary arteries. (
  • In functional test of primary haemostasis, extracts of S. brachyodon have prevented platelet aggregation in nanomolar concentration (21 nM), thus showing potential in prevention of thrombus formation as functional food or dietary supplement. (
  • Various medical devices are used in platelet aggregation which allows precise control over the dynamic differential rate of blood flow control along with the extent of platelet thrombus formation. (
  • The model and simulation framework can be further adapted to simulate initial thrombus formation involving multiple flowing platelets as well as deposition and adhesion onto blood vessels. (
  • PI3-kinase plays a role in regulating NADPH oxidase-generated superoxide in platelets and, by altering the bioactivity of platelet NO, may be a potential method for reversing platelet aggregation and thrombus formation. (
  • 4 The released ADP can interact with P2Y 1 and P2Y 12 (formally known as P 2T ) receptors on platelets and induce platelet aggregation, 5-7 which contributes to normal hemostasis and to thrombus formation. (
  • In the Chandler tube apparatus the thrombus formation time of recalcified sheep whole blood and platelet-rich plasma was significantly prolonged in the presence of these agents with the exception of hyoscine. (
  • The development and progression of CVD lies in the interactive processes of atherosclerotic lesions and thrombus formation, an interaction established primarily by platelet-endothelial binding ( 3 ). (
  • Receptor ligation with collagen, in company with other agonist/receptor interactions, augments inside out signaling pathways leading to platelet aggregation and thrombus formation. (
  • Under conditions of relatively low shear, aggregation is mediated by fibrinogen via αIIbβ3 receptors. (
  • Platelets express the receptors for adiponectin. (
  • It is known that ATP can interact with P2X 1 receptors on platelets, causing a transient Ca 2+ mobilization, 8,9 but this does not result in platelet aggregation, and the importance of P2X 1 receptors to overall platelet function is unknown. (
  • It is also known that ATP acts as an antagonist of the effects of ADP at P2Y 1 and P2Y 12 receptors 10,11 and that high concentrations can inhibit ADP-induced platelet aggregation. (
  • 05). Endothelin-1 increased pHi through endothelin A-receptors (effect blocked by the specific antagonist BQ-123) but had no significant effect on [Ca2+]i or aggregation. (
  • Increasing numbers of unblocked receptors were required for an aggregation response with a decreasing concentration of ADP. (
  • Conclusions These data demonstrate that the morning increase in platelet aggregation is not accompanied by expression of activation-dependent platelet surface receptors and suggest that the increase in whole-blood aggregation may be primarily due to the increases in catecholamine levels, platelet count and hemocon-centration. (
  • Chapter 1 is a review and critique of the literature on platelet structure and function, transient receptor potential vanilloid-1 (TRPV1) channels and cannabinoid (CB) receptors in health and disease, vanilloids and their clinical applications, the manifestations of systemic lupus erythematosus (SLE), and the role platelets in SLE. (
  • However, blocking TRPV1 and CB2 receptors appear to enhance OLDA and CAP inhibitory action on platelets. (
  • After excluding a definite role for TRPV1, CB1 and CB2 receptors in the action of vanilloid on platelets, other possible mechanisms were investigated in Chapter 3. (
  • Thus, the focus of this thesis was whether vanilloids exert their action on platelets by interfering with 1) ADP receptors by measuring vasodilatorstimulated phosphoprotein (VASP) phosphorylation level, dense- (5- hydroxytryptamine (5-HT)) release, and/or α-granules (platelet factor 4 (PF4) and β- thromboglobulin (β-TG)) release, and/or 2) the AA metabolic pathway in platelets. (
  • Calcium-dependent linkage formation between activated receptors and bivalent fibrinogen follows, resulting in platelet aggregation. (
  • In addition, platelet spreading on immobilized fibrinogen was incomplete, and platelet aggregation assays confirmed a general defect in integrin-dependent platelet aggregation in patients with myelodysplastic syndromes. (
  • The force field, parametrized in two different interaction scales, is calculated by correlating with the platelet contact area measured in vitro and the detaching force between αIIbβ3 and fibrinogen. (
  • Frojmovic, M. M. Flow cytometric analysis of platelet activation and fibrinogen binding. (
  • Potent inhibitors of platelet aggregation based upon the Arg-Gly-Asp-Phe sequence of fibrinogen. (
  • Hydroxyethyl starch (HES) solutions alter blood coagulation, mainly platelet function and fibrinogen polymerization. (
  • We have also demonstrated that fibrinogen, an activator of integrin αIIbβ3, enhances SERT activity in human platelets and that integrin αIIbβ3 interacts directly with the C terminus of SERT. (
  • This involves a conformational change in the extracellular domain of the integrin platelet glycoprotein (GP)IIb-IIIa facilitating the binding of soluble fibrinogen and enabling the formation of cross bridges between platelets essential for platelet aggregation. (
  • Its N-terminal sequence has high similarity to disintegrins isolated from different snake venoms, which are known to bind to cellular integrins such as the GPIIb/IIIa fibrinogen receptor on platelets. (
  • 8 Fibrinogen (0.4 mg/mL) was added to washed platelet suspensions before stimulation with the platelet agonists. (
  • 2) Secretion of proaggregatory mediators such as ADP, ATP, platelet factor 4 (PF4), beta thromboglobulin (beta-TG), thromboxane A 2 (TXA 2 ), fibrinogen and thrombospondin which are followed by the translocation of the alpha-granule membrane protein P-selectin (CD 62) to the platelet surface. (
  • Our data provide novel aspects on the molecular pathology of impaired platelet function in myelodysplastic syndromes and suggest a mechanism of defective integrin αIIbβ3 signaling that may contribute to the hemorrhagic diathesis observed in these patients. (
  • We employed whole blood platelet aggregation analysis based on impedance as well as determination of ATP release from platelet granules detected by a chemiluminescence method. (
  • Whole blood platelet analysis detected platelet dysfunction which may be associated with bleeding and thrombotic risks in uremia. (
  • Blood will be drawn via venopuncture for laboratory studies (whole blood platelet aggregation, von Willebrand Factor antigen levels and activity). (
  • On visit 2, whole blood platelet aggregation will be re-measured and questionnaires filled out. (
  • Methods Expression of seven platelet surface antigens (including P-selectin, activated GPIIb-IIIa and GPIb-IX), whole-blood platelet aggregation, platelet count and hematocrit were measured before and after arising in 17 normal volunteers. (
  • Thus, the aim of the present study was to examine the effects of propolis extracts on human platelet aggregation in vitro and to identify the nature of the compounds responsible for the antiplatelet activity. (
  • Microsomes prepared from rabbit or pig aortas transformed endoperoxides (PGG2 or PGH2) to an unstable substance (PGX) that inhibited human platelet aggregation. (
  • Additionally, using pharmacological blockers of SERT and the vesicular monoamine transporter (VMAT), we have identified a role for ongoing 5-HT release and SERT activity in efficient human platelet aggregation. (
  • Carbon monoxide (CO) inhibits human platelet aggregation triggered with threshold levels of agonists like arachidonate, ADP, collagen, thrombin, or the prostaglandin endoperoxide analogue U46619. (
  • The aim of this study was to investigate the effects and mechanisms of action of horse chestnut on the contraction of bovine mesenteric veins and arteries, and human platelet aggregation. (
  • ADP-induced human platelet aggregation was significantly reduced by horse chestnut. (
  • Human platelet aggregation is reduced by horse chestnut. (
  • Platelet hyperactivity plays an important role in arterial thrombosis and atherosclerosis. (
  • In addition, if a drug could also inhibit platelet aggregation, it would be very helpful because it prevents stent thrombosis associated with DES 10 . (
  • Hyperglycaemia is associated with increased platelet aggregation that increases the risk of thrombosis in people with type-2 diabetes and cardiovascular disease. (
  • The aim of the portrayed invention is to develop and make new drugs for the primary- and secondary prophylaxis of thrombosis complications as well as the general treatment of cardiovascular diseases available, using inhibitors of the multidrug resistance protein (MRP) in human platelets, more specifically of MRP4. (
  • The patent awarded covers the basic composition of TP-9201, a platelet aggregation inhibitor , and related compositions for the treatment of thrombosis," said Dr. (
  • It is a process in which platelets adhere to each other at sites of vascular injury, which has long been recognized as critical for hemostatic, plug formation and thrombosis. (
  • Besides resolving some questions concerning the activation of platelets by shear forces, this study further implicates fluid mechanical factors in thrombosis and arterial disease. (
  • Immunohistochemical staining against podoplanin and intratumoral platelet aggregates was performed in brain tumor specimens of 213 patients (mostly high-grade gliomas [89%]) included in the Vienna Cancer and Thrombosis Study (CATS), a prospective observational cohort study of patients with newly diagnosed cancer or progressive disease aimed at identifying patients at risk of VTE. (
  • Platelet activation plays a major role in hemostasis and thrombosis. (
  • Since the thrombin clotting times in platelet-poor plasma were unaffected in their presence, it is suggested that the inhibitory effect of these substances on both platelet clumping and the experimental thrombus development is not an anticoagulant action but that it is related to their ability to prevent the uptake of serotonin by platelets, and that 5-HT may have a secondary and potentiating role in thrombosis. (
  • The role of platelets in arterial thrombosis is well known ( 9 ). (
  • Accordingly, platelets act as a bridge between the inflammatory processes characteristic of atherosclerosis and thrombosis ( 20 ). (
  • Conspicuously, PCA did not inhibit platelet aggregation induced by other endogenous agonists like collagen, thrombin, or ADP that are important in both pathological thrombosis and normal hemostasis. (
  • Platelet α-granules have an important role in hemostasis as well as thrombosis. (
  • HOUSTON , April 8, 2019 /PRNewswire/ -- Platelet testing and research company Aggredyne, Inc. has received U.S. Food and Drug Administration (FDA) clearance for its unique AggreGuide A‑100® ADP Assay testing cartridge, a cost-effective in vitro diagnostic device used to measure the effect of various antiplatelet medications that target the platelet P2Y12 receptor. (
  • Recently, Liu and his colleagues put forward that chrysin in propolis performs antiplatelet activity via inhibiting platelet alphaIIbbeta3-mediated signaling pathway [ 22 ]. (
  • Antiplatelet activity was related to antioxidant capacity (r=0.7014, p=0.0352) indicating that prevention of aggregation is not caused by an individual component, but it is rather a result of synergistic effect of polyphenols. (
  • Therefore, development of effective antiplatelet agents is necessary for ameliorating platelet-related diseases. (
  • However, blocking cyclic AMP formation with 2′5′-ddAdo, an inhibitor of adenylate cyclase, greatly reversed the antiplatelet activity of MP407 and related platelet-activating pathways. (
  • Taken together, MP407 may be a potential candidate or lead compound for developing novel antiplatelet or antithrombotic agents for platelet hyperactivity-triggered disease therapy. (
  • The antiplatelet effect of clopidogrel, as assessed by ADP-induced platelet aggregation, was measured by Multiplate impedance aggregometry. (
  • The results indicated that 3d had a potent antiplatelet aggregation activity in both the ADP- and AA-induced platelet aggregation. (
  • The model accurately predicted the order of potency for three antiplatelet therapies, donor-specific aggregate size, and donor-specific response to antiplatelet therapy as compared to microfluidic experiments of platelet aggregation. (
  • Antiplatelet agents are medicines that reduce the ability of platelets to stick together (called platelet aggregation) and inhibit the formation of blood clots. (
  • Platelet aggregation studies test the clumping response of platelets to various platelet activators (eg, ADP, collagen, arachidonic acid, thrombin, epinephrine, ristocetin) as continuously recorded by a light transmission aggregometer. (
  • Platelet aggregation induced by ADP was also abrogated by NPP-BJ, whereas thrombin-induced platelet aggregation was only slightly attenuated. (
  • There were no significant changes in platelet aggregation induced by thrombin receptor-activating peptide and in any parameter of rotational thrombelastometry. (
  • Here, using SERT-deficient mice, we have established a role for constitutive SERT expression in efficient ADP- and thrombin-triggered platelet aggregation. (
  • Adenosine (1.1 µM) was equally effective in antagonizing 5-HT, ADP and thrombin-induced platelet aggregation. (
  • preventive administration of NADPH in the rats can remarkably inhibit Thrombin-induced platelet aggregation. (
  • However, endothelin-1 blunted thrombin-induced platelet aggregation in normotensive subjects but not in hypertensive patients. (
  • Aggregation agonists may be grouped as strong agonists, such as thrombin, and weak agonists, such as ADP. (
  • To clarify the influence of sevoflurane on thrombin-induced platelet aggregation, halothane was used as a positive control, and isoflurane was used as a negative control. (
  • citation needed] In an unknown fashion, the antibiotic ristocetin causes von Willebrand factor to bind the platelet receptor glycoprotein Ib (GpIb), so when ristocetin is added to normal blood, it causes agglutination of fixed platelets or initiates the initial agglutination phase of aggregation of live platelets. (
  • Despite normal agonist receptor expression, calcium flux, and granule release upon activation, the activation capacity of integrin αIIbβ3 was diminished in myelodysplastic syndrome platelets. (
  • Triggering Receptor Expressed on Myeloid cells-1: a new player in platelet aggregation. (
  • Another member of the TREM family, The Triggering receptor expressed on myeloid cells Like Transcript-1 (TLT-1) is exclusively expressed in platelets and promotes platelet aggregation. (
  • A proposal on the nature of the binding interaction between the Asp-carboxylate of RGDX mimetics and the platelet GP IIb-IIIa receptor. (
  • This study assessed whether platelet hyperreactivity to epinephrine in hypercholesterolemia is associated with higher alpha 2-adrenergic receptor density or affinity for epinephrine. (
  • In these subgroups plasma total and levels of low-density lipoprotein (LDL) cholesterol were inversely correlated with platelet aggregation but directly correlated with platelet receptor density. (
  • Platelet alpha 2-adrenergic receptor density is increased in hypercholesterolemia and directly correlates with plasma total and levels of LDL cholesterol, providing at least a partial explanation for the enhanced platelet response to epinephrine that is observed in hypercholesterolemia. (
  • These data demonstrate the aqueous stem extract of T. sarmentosa significantly suppressed platelet aggregation through P2Y 1 and P2Y 12 receptor signal pathways. (
  • In isolated human platelets, PCA decreased SIPA and attenuated accompanying platelet activation, including intracellular calcium mobilization, granule secretion, and adhesion receptor expression. (
  • Platelet receptor GPVI plays an important role in platelet firm adhesion to site of vascular injury. (
  • Data presented here demonstrated that progressive shedding of surface adhesion receptor GPVI can affect its functional activities in stored platelets. (
  • Thereby considering the crucial role of GPVI in platelet adhesion to the site of injury, whether the therapeutic efficacy of banked platelet products could be influenced by storage-dependent shedding of this receptor, remains to be answered in future studies. (
  • Gardiner EE, Arthur JF, Berndt MC, Andrews RK (2005) Role of calmodulin in platelet receptor function. (
  • The psychotomimetic analgesic phencyclidine (PCP), which binds to a high affinity site on the neuronal N-methyl-D-aspartate (NMDA)-sensitive glutamate receptor, has previously been found to bind to platelets with high affinity and to specifically delay the onset of epinephrine-stimulated platelet aggregation (Jamieson et al. (
  • We have now shown that the rank order of binding affinities of 14 synthetic PCP analogs at the high affinity binding site on platelets does not parallel the rank order of their affinities in binding to rat brain membranes, indicating that the high affinity PCP binding sites in platelets is distinct from the neuronal NMDA receptor. (
  • Furthermore, (+)MK-801, which binds to the same high affinity binding site in neurons as does PCP, failed to inhibit epinephrine-stimulated platelet aggregation, further suggesting that the site at which PCP acts in platelets is not related to the NMDA-type glutamate receptor. (
  • In addition, evidence data showed that propolis coated Co-Cr could significantly reduce adhesion of platelets [ 23 ]. (
  • Our model indicates that assuming a rigid-platelet model, underestimates the contact area by 89% and the detaching force by 93% as compared to a model that takes into account the platelet deformability leading to a prediction of a significantly lower attachment during recruitment. (
  • Platelet aggregation in response to epinephrine was significantly higher in patients with hypercholesterolemia than in control subjects. (
  • AEE significantly inhibited ADP and AA-induced platelet aggregation in vivo. (
  • All three small molecules significantly attenuated platelet aggregation as did the antibody 8C10, although 3H12 had a weaker effect. (
  • Scanning electron microscopy and radiolabeled platelet studies revealed that platelet adherence to T. cruzi -infected human endothelial cells was significantly increased when compared to controls ( P = 0.024). (
  • As GPVI expression is significantly modulated by ectodomain shedding, this study aimed to examine whether GPVI shedding functionally affects collagen-mediated platelet activation during storage. (
  • The increasing levels of GPVI shedding during storage were in reverse correlation with collagen-induced platelet aggregation (r = − 0.82, p = 0.0004) which was significantly reducing during storage. (
  • Platelet adhesion to collagen matrix significantly decreased post-storage while it was also reversely correlated with the levels of GPVI shedding during 5 days storage of platelets (r = − 0.69, p = 0.002). (
  • My previous Masters work showed that the endovanilloids, OLDA and NADA, as well as the high concentrations (100-25 μM) of plant-derived vanilloid, CAP, significantly inhibit in vitro ADP-induced platelet aggregation. (
  • Mean platelet aggregation was significantly lower in coronary venous blood than aortic blood, using epinephrine and ADP as aggregating agents. (
  • High-intensity intermittent exercise increases adenosine hydrolysis in platelets and lymphocytes and promotes platelet aggregation in futsal athletes. (
  • Platelet inhibitory effect of clopidogrel in patients treated with omeprazole, pantoprazole, and famotidine: a prospective, randomized, crossover study. (
  • For this reason aim of the present study is to evaluate the levels of platelet aggregation during the pharmacological shift from clopidogrel to ticagrelor performed with or without a loading starting dose of the newer drug. (
  • Plavix (clopidogrel), a platelet aggregation inhibitor , is BMS' largest selling product and continues to make substantial year-on-year sales growth. (
  • The thienopyridine anti-platelet drugs, such as clopidogrel, require metabolic activation in vivo to effectively block platelet aggregation. (
  • Conditions were optimized whereby washed human platelets can be incubated in the presence of an individual, recombinant CYP and clopidogrel. (
  • rs4986893) null alleles are responsible for the phenotypes of poor CYP2C19 enzyme function, hence adversely affecting the ability of clopidogrel to inhibit platelet aggregation. (
  • To date, there is limited data on CYP2C19 prevalence rates in a multiracial Malaysian population with coronary artery disease planned for percutaneous coronary intervention (PCI), and their impact on clopidogrel-mediated platelet aggregation (CPA). (
  • Rifampicin increases the inhibitory effect of clopidogrel on platelet aggregation (PA). (
  • Intracoronary shear-related up-regulation of platelet P-selectin and platelet-monocyte aggregation despite the use of aspirin and clopidogrel. (
  • At 25 mg/L to 300 mg/mL, the water extract propolis (WEP) inhibited three agonists-induced platelet aggregations in a dose-dependent manner. (
  • The interaction of Gas6 with Mer, Axl, and Tyro-3 is important in platelet degranulation and aggregation in response to known agonists. (
  • The response of platelets to a complex signal of pro-clotting agonists determines the stability and size of the resulting clot. (
  • Finally, the LKMC method was incorporated within a multiscale model to simulate platelet aggregation including platelet signaling (neural network model), blood flow (lattice Boltzmann method), and the release of soluble platelet agonists (finite element method). (
  • This study, however, was performed on the platelet aggregation induced by weak agonists such as ADP and epinephrine. (
  • Platelet aggregation was studied using a light transmission aggregometer (Dual Aggregometer, Chrono-Log Corporation, Havertown, PA, USA) and recorded for 3 min after stimulation of platelets with the indicated platelet agonists as described. (
  • These agonists induce platelet adhesion, activation and aggregation leading to rapid occlusion of the aperture and cessation of blood flow termed the closure time (CT). (
  • In the present work, we fractionated B. asper venom in order to investigate the possible presence of inhibitors of platelet aggregation. (
  • Blocking vWF and integrin adhesion pathways prevented both aggregation and phagocytosis. (
  • The stimulatory effect of endothelin-1 on pHi but not on [Ca2+]i or aggregation suggests that in platelets endothelin-induced signaling pathways other than phospholipase C may be involved. (
  • Our results suggest that a loss of activity of endogenous inhibitorymechanisms could contribute to the increased platelet reactivity in ApoE-/- mice, and that this phenomenon occurs early in the intermediate stage of the atherosclerotic process. (
  • Increased platelet reactivity is one mechanism that may explain the enhanced risk of thromboembolism in hypercholesterolemia. (
  • Gordon JL, Bowyer DE, Evans DW, Mitchinson MJ (1973) Human platelet reactivity during surgical diagnostic procedures. (
  • It has been reported that phenols (anthocyanins) from the chokeberry decreased blood pressure, lowered plasma lipid concentration and peroxidation, and reduced blood platelet reactivity, which makes them potentially interesting pharmaceuticals for cardiovascular therapy [5, 6]. (
  • In conclusion, carvedilol, a nonselective BB, reduces residual platelet reactivity in patients with ACS compared with the selective BB, metoprolol. (
  • Abstract Platelets from two patients with essential thrombocythemia failed to aggregate or release serotonin in response to concentrations of epinephrine that aggregated platelets from normal controls. (
  • The ristocetin-induced platelet aggregation (RIPA) is an ex vivo assay for live platelet function. (
  • Intravenous infusion of PGI 2 also failed to inhibit platelet aggregation ex vivo in 18- to 20-week-old ApoE-/- mice. (
  • When considering the possible effects of ATP on platelets in vitro and in vivo, the presence of enzymes present on blood cells and endothelial cells and in plasma that metabolize ATP must be taken into account. (
  • Mer regulates macrophage activation, promotes apoptotic cell engulfment, and supports platelet aggregation and clot stability in vivo. (
  • Mice lacking either Gas6 or Mer protein have impaired platelet aggregation in vitro and diminished clot stability in vivo. (
  • Larsson PT, Hjemdahal P, Olsson G, Egberg N, Hornsta G. (1989) Altered platelet function during mental stress and adrenaline infusions in humans: evidence for increased aggregability in vivo as measured by filtragometry. (
  • Bergmeier W, Piffath CL, Cheng G, Dole VS, Zhang Y, von Andrian UH, Wagner DD (2004) Tumor necrosis factor-alpha-converting enzyme (ADAM17) mediates GPIbalpha shedding from platelets in vitro and in vivo. (
  • The work herein examines in vitro platelet aggregation in response to fluid shearing motion. (
  • 1 Because platelet count is considered a major determinant of in vitro platelet aggregation, 1 , 2 platelet counts in the two PRP samples (from the index patient and the normal control) should be adjusted to the same value, using autologous platelet-poor plasma (PPP) for correct dilution. (
  • Light transmission aggregometry was performed at randomization (T0) and at 30-day follow-up (T30), and the results were expressed as a percentage of maximum platelet aggregation (MPA). (
  • The companion A-100 AA assay cartridge, used to determine the effect of aspirin on platelet activity, and the A-100® instrument received FDA clearance in 2013. (
  • Recovery time of platelet function after aspirin withdrawal. (
  • Diminished ATP release to arachidonic acid (an aspirin-like defect) in uremic patients may result in platelet associated bleeding. (
  • Only 28% of all patients in the trial, sponsored by Ortho Biotech Clinical Affairs, were on a platelet aggregation inhibitor such as aspirin. (
  • The investigators hypothesize that patients with Chronic Kidney Disease compared with non-Chronic Kidney Disease have reduced platelet aggregation and poor platelet inhibitory response to aspirin. (
  • Notably, aspirin and eugenol produce similar pharmacological effects especially on inflammation and platelet aggregation. (
  • The purpose of the study was to determine the influence of fluvastatin and atorvastatin on platelet aggregation in patients treated with aspirin and plavix after coronary stenting. (
  • A drug or agent which antagonizes or impairs any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system. (
  • Prostaglandin endoperoxides cause platelet aggregation possibly through the generation by platelets of thromboxane A2. (
  • Our results demonstrated that MP407 dose-dependently inhibited collagen-induced platelet aggregation, thromboxane B2 (TXB2) production, intracellular Ca2+ mobilization, platelet membrane GPIIb/IIIa expression, and the phosphorylation of Akt, GSK3β, p38MAPK, and phospho (Ser) PKC substrate (p47). (
  • Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system. (
  • Imidazole, a drug known to inhibit synthesis of both prostacyclin and thromboxane, failed to affect platelet aggregation. (
  • 10 reported that sevoflurane inhibited platelet aggregation by suppressing the formation of thromboxane A 2 , concluding that the inhibitory effect of sevoflurane could be mediated by a decrease in cyclooxygenase activity. (
  • Factors such as growing number of surgical procedures, rising awareness among healthcare professionals (related to the benefits offered by platelet aggregation testing in disease diagnosis), large number of patients undergoing cardiovascular surgeries, and increasing prevalence of orthopedic, urological, and bleeding disorders are offering high-growth opportunities for players active in the North American platelet aggregation devices market. (
  • Tumor cell-induced platelet aggregation (TCIPA) facilitates the embolization of the vasculature with tumor cells and the formation of metastatic foci. (
  • Reduced β2-GPI is associated with increased platelet aggregation and activation in patients with prolonged isolated thrombocytopenia after allo-HSCT. (
  • The company is also developing additional assays to be used with its instrument(s) in the anti-platelet therapy field as well as in related disease states. (
  • Patients allocated in the two study arms will receive the same anti platelet treatment, except for the administration of the loading dose, which will be only administered to patients allocated in Group 2. (
  • Higher coronary in-stent thromboses and bleeding complications on anti-platelet agents are more common in Chronic Kidney Disease vs. non-Chronic Kidney Disease patients. (
  • Accomplishing these aims will provide pilot data to power future studies of targeted anti-platelet agent treatments in Chronic Kidney Disease in order to improve cardiovascular outcomes. (
  • Venous blood (32 ml) was obtained by antecubital venipuncture from healthy volunteers who had not taken any drug known to affect platelet aggregation for at least 2 weeks. (
  • Platelet aggregation studies were performed on aortic and coronary venous blood of 28 patients with coronary artery disease. (
  • Platelet counts were lower in coronary venous blood. (
  • Platelet aggregation was lower in aortic and coronary venous blood in 12 patients who were taking propranolol than in 16 patients not taking propranolol. (
  • Platelet aggregation is lower in coronary venous blood in patients with coronary disease. (
  • Propranolol decreases aggregation in aortic and coronary venous blood. (
  • Lower platelet aggregation in coronary venous blood may be related to removal of reactive platelets or formation of platelet aggregates in diseased coronary vasculature. (
  • Here, we examined the effects of Exisulind on neointimal formation after balloon injury and its mechanisms of action in VSMCs, endothelial cells, and platelets. (
  • In order to study the mechanisms of platelet consumption in liver xenotransplantation, we have developed an in vitro system to examine the interaction between pig endothelial cells with baboon platelets and to thereby identify molecular mechanisms and therapies. (
  • Phagocytosis was evaluated by direct observation of CFSE labeled-platelets, which are incubated with endothelial cells under confocal light microscopy. (
  • However, pig hepatocytes, liver sinusoidal and aortic endothelial cells (GTKO and Gal+) all induced moderate aggregation of baboon platelets. (
  • Importantly, pig liver sinusoidal endothelial cells efficiently phagocytosed baboon platelets, while pig aortic endothelial cells and hepatocytes had minimal effects on platelet numbers. (
  • Conclusions: Although pig hepatocytes and aortic endothelial cells directly caused aggregation of baboon platelets, only pig liver endothelial cells efficiently phagocytosed baboon platelets. (
  • The interaction between platelets and endothelial cells occurs in two manners: activated platelets unite with intact endothelial cells, or platelets in resting adhere to activated endothelium. (
  • Since those antigens on human plasma vWF are not changed to those of the donors after ABO-mismatched bone marrow transplantation, we concluded that plasma vWF with the blood groups is derived from endothelial cells, but not from megakaryocytes (platelets). (
  • Platelet proteome analysis reveals integrin-dependent aggregation defects in patients with myelodysplastic syndromes. (
  • Proteins identified with lower concentrations, such as Talin-1, Vinculin, Myosin-9, Filmain-A, and Actin play critical roles in integrin αIIbβ3 signaling and thus platelet aggregation. (
  • Here, I describe a method to study platelet integrin activation and granule release using flow cytometry, and a complementary method to study platelet aggregation using a dedicated platelet aggregometer. (
  • Consistent with these findings, knockout mice lacking integrin β3 displayed diminished platelet SERT activity. (
  • The companion A-100® instrument uses laser light scattering to quickly quantify platelet aggregates in the sample. (
  • Seventeen of the 30 samples showed platelet aggregates in the counting chamber. (
  • Significant differences in platelet counts were associated with the presence and size of aggregates and time since bleeding. (
  • CONCLUSION For the first time, deaggregation of feline platelet aggregates could be demonstrated as a reversible effect of platelet aggregation. (
  • PATIENTS AND METHODS: We measured serum hcy and ADP-induced platelet aggregation and plasma tissue factor as a major activator of the coagulation cascade in hemodialysis (HD), peritoneal dialysis (PD) and early stage chronic renal failure (early stage CRF) patients who are not receiving dialysis and compared with those of control. (
  • The combination of these methods represents a rapid and cost-effective strategy to provide mechanistic insight on the type of platelet response mediated by the bacteria. (
  • Subjects/Methods: Platelet aggregation and circulating adiponectin, sCD40L and P-selectin were determined in 30 controls and 30 patients with MS. (
  • Methods and Results- Incubation of platelets with PI3-kinase inhibitors led to a dose-dependent increase in platelet NO and cGMP levels that were temporally related to the period of platelet disaggregation. (
  • Deerfield Beach, FL -- ( SBWIRE ) -- 02/09/2017 -- Platelet aggregation is defined as the clumping together of platelets in the blood. (
  • Adenosine and adenosine monophosphate, which are known to inhibit platelet aggregation induced by ADP, also block that induced by latex. (
  • It has been widely known that platelets play important roles in both hemostasis and pathogenesis of CVD such as acute coronary syndrome [ 4 ]. (
  • Esposito, Giovanni 2018-07-01 00:00:00 Platelet aggregation plays a pivotal role in acute coronary syndrome (ACS). (
  • Platelet aggregation plays a pivotal role in acute coronary syndrome (ACS). (
  • Seven tubes are required for full aggregation and secretion testing. (
  • With some aggregometers, the secretion of platelet granules, another indicator of platelet function, may also be evaluated simultaneously by measuring the release of ATP by the aggregating platelets. (
  • Platelet secretion defects can provide greater diagnostic sensitivity than platelet aggregation testing alone. (
  • Furthermore, the activation of platelets was also related to circulation and vascular damage in patients with hypertension and diabetes [ 6 ]. (
  • Objective- While much is known about the normal activation of platelets, there have been few observations demonstrating reversibility of the aggregation process. (
  • The activation of platelets involves a series of coordinated events that are tightly regulated to maintain hemostasis. (
  • Dietary supplements (Vitamin e and fish oil) known to affect platelet function will be assessed and patients on those will be asked to discontinue these. (
  • Participants with also be asked to not eat foods known to affect platelet function (coffee, chocolate, grapes, and alcohol) 48 hours prior to sample collection on visit 1. (
  • However, this practice could also affect platelet function independently of the induced change in platelet count, as PPP may contain substances affecting platelet function that are released by platelets or other blood cells during high-speed centrifugation of blood samples necessary to obtain PPP. (
  • Experimental pancreatitis caused in dogs has been found to affect platelet function and size [ 2 ]. (
  • Here we describe for the first time the isolation and functional characterization of a soluble phosphodiesterase from Bothrops jararaca venom, which shows amino acid sequence similarity to mammalian nucleotide pyrophosphatase/phosphodiesterase 3 (NPP3), and inhibits ADP-induced platelet aggregation. (
  • We hypothesized that podoplanin, a sialomucin-like glycoprotein, increases the risk of VTE in primary brain tumors via its ability to induce platelet aggregation. (
  • Platelet function analysis utilizing platelet-rich plasma and optical density based aggregometry fails to identify patients at risk for uremia associated complications. (
  • Platelet aggregation is measured by means of Multiple Electrode Aggregometry (MEA) and Light Transmission Aggregometry (LTA). (
  • Blood was subjected to blood gas analysis, assessment of platelet function [with multiple electrode aggregometry (MEA)], and clot formation (with rotational thrombelastometry). (
  • Reference values of platelet aggregometry in healthy subjects. (
  • Platelets' aggregation state was also evaluated with Multiplate ® aggregometry analyzer in 48 male subjects living in a specific area of the Veneto region with high PFAS environmental pollution, and compared with 30 low-exposure control subjects. (
  • Light transmission aggregometry is the most widely used laboratory method to screen patients with suspected abnormalities of primary hemostasis due to inherited or acquired defects of platelet function. (
  • Platelet activation can be estimated through flow cytometry, measurement of platelet-specific proteins such as beta-TG, PF4 and soluble P-selectin in plasma and TXA 2 metabolites in both plasma and urine dose-response and aggregometry [ 8 ]. (
  • Platelet-rich plasma was prepared and incubated in vitro with different concentrations of the tested extracts and components of flavonoids. (
  • The addition of iodoacetate and 2,4-dinitrophenol in appropriate concentrations to the PRP, prior to the addition of the latex, blocks platelet aggregation and phagocytosis. (
  • Making reference to actual aggregation curves of human plasma for various ADP concentrations, the authors have modelled the rate at which the density of aggregated platelets continues to increase in the aggregation process. (
  • A randomised cross-over study compared the acute effects of a high GI high carbohydrate (HGI-HC), a low GI high carbohydrate (LGI-HC) and a low GI moderately high in protein and fat (LGI-MPF) meal on postprandial platelet aggregation, glucose, insulin and triglyceride concentrations. (
  • Moreover, aggregation in the shear field disappears at sufficiently low platelet concentrations (below about 60,000/mm('3) plasma), suggesting that chemical release or leakage from platelets may mediate shear-induced aggregation. (
  • Enhanced platelet aggregation and activation markers are found in the metabolic syndrome associated to low adiponectin concentrations. (
  • 1,2 The amount of ATP released from erythrocytes is approximately 10 times the amount of ADP, 3 and ATP and ADP in platelet secretory granules are present in approximately equimolar concentrations. (
  • Effects of angiotensin II and endothelin-1 on platelet aggregation and cytosolic pH and free Ca2+ concentrations in essential hypertension. (
  • The aims of this study were to determine the relations between platelet free calcium concentrations ([Ca2+]i), intracellular pH (pHi), and aggregation and to assess the effects of angiotensin II (Ang II) and endothelin-1 on these platelet parameters in normotensive subjects and hypertensive patients. (
  • These results confirm that acute inhalative exposure to high PM(10) concentrations during hay storage activity leads to a systemic inflammatory reaction, endothelial activation, and platelet aggregation. (
  • These include enzymes that convert ATP to ADP and ADP to AMP (NTPDase-1, also known as ATP diphosphohydrolase, CD 39 and EC, 13,14 ATP to AMP and ADP to AMP (5′-monophosphate phosphoanhydrolase/phosphodiesterase, NMPP), 15 and AMP to adenosine (5′-nucleotidase), 13 the latter being an inhibitor of platelet aggregation. (
  • All of our data are compatible with the hypothesis that prostacyclin is an inhibitor of platelet aggregation. (
  • It is similar to the ristocetin cofactor assay but has the added benefit in that it helps in the diagnosis of type 2B/pseudo von Willebrand disease (vWD) and Bernard-Soulier syndrome because it uses patient's live endogenous platelets, whereas ristocetin cofactor assay tests the function of only the vWF and not the platelets. (
  • In the present study, we assessed whether the endogenous platelet inhibitory mechanisms are altered in the early to moderate stages of the atherosclerotic process. (
  • In this study, the role of PI3-kinase in the regulation of endogenous platelet NO and the relevance to platelet function was determined. (
  • It has been shown that vanilloid-like agents, including plant-derived vanilloids (capsaicin (CAP) and dihydrocapsaicin (DHC)), and endogenous vanilloids (Narachidonoyl-dopamine (NADA) and N-oleoyldopamine (OLDA)), individually inhibit in vitro aggregation in platelets obtained from healthy donors. (
  • The test can help diagnose problems with platelet function. (
  • Conditions associated with decreased platelet aggregation include suspected hereditary and acquired disorders of platelet function. (
  • The test can help diagnose problems with platelet function and determine whether the problem is due to your genes, another disorder, or a side effect of medicine. (
  • The essential contribution of the antidepressant-sensitive serotonin (5-HT) transporter SERT (which is encoded by the SLC6A4 gene) to platelet 5-HT stores suggests an important role of this transporter in platelet function. (
  • We aimed to measure platelet function and its relationship with β2-GPI in prolonged isolated thrombocytopenia (PT) after allogeneic hematopoietic stem cell transplantation (allo-HSCT). (
  • Here, we investigated the effect of PFOA exposure on platelets' function, a key player in atherosclerosis process. (
  • We hypothesized that adiponectin modulates platelet function. (
  • In addition, NO is a known potent inhibitor of platelet function. (
  • The highly reactive oxygen species superoxide is produced by activated platelets and also acts to regulate platelet function. (
  • Furthermore, a physiologic role for the Mer tyrosine kinase has been described for the normal function of platelets. (
  • Many investigators are interested in the relationship between mental stress and platelet function, coagulation and fibrinolysis [1, 2], since several lines of evidence suggest that atherosclerotic cardiovascular events may be related to mental stress. (
  • The neural network model for platelet signaling was trained on patient-specific, experimental measurements of intracellular calcium enabling patient-specific predictions of platelet function in flow. (
  • According to this protocol, individuals who had been taking drugs known to interfere with platelet function for the 15 days previous to blood sampling were not included in the study. (
  • Chapters two through five present the related background, research experiments and data generated that detail the mechanistic investigations of the inhibitory effects of vanilloids on platelet function. (
  • In recent years a number of dietary sources inhibiting platelet function have been reported, but so far, due to the rather confusing array of conflicting evidence, the exact relationship between diet and platelet function remains unresolved [2]. (
  • 1) Studies on the isolation and structure-function relationship of snake venom proteins modulating interaction between von Willebrand factor (vWF) and platelets. (
  • Objective In the present study, we evaluated the alterations of platelet function in patients suffering from acute edematous pancreatitis using the recently developed platelet function analyzer PFA-100 TM . (
  • The diagnosis of this condition can be done via the following: Flow cytometry Bleeding time analysis Platelet aggregation function study: This condition may involve the alpha granules or the dense granules. (
  • We developed a multiscale model to simulate the dynamics of platelet aggregation by recruitment of unactivated platelets flowing in viscous shear flows by an activated platelet deposited onto a blood vessel wall. (
  • Thrombomodulin alfa prevents the decrease in platelet aggregation in rat models of disseminated intravascular coagulation. (
  • Disseminated intravascular coagulation (DIC), a deadly complication characterized by uncontrolled hypercoagulation, causes a decrease in the platelet count and impairs platelet aggregation. (
  • Our specific aim is to characterize shear-induced aggregation by means of kinetic measurements. (
  • Kinetic data from shear-induced aggregation indicate two population balance measures are important: the particle collison efficiency, (epsilon), and the particle void volume fraction, (phi). (
  • Therefore, we investigated the effect of shear-induced platelet activation on red blood cell (RBC) aggregation. (
  • In our study, an increase in RBC aggregation indices (critical shear stress (CSS) and aggregation index (AI)) by shear-induced platelet activation was observed. (
  • Platelet disorders and von Willebrand disease. (
  • 0002] Binding of platelets to von Willebrand factor (vWF) in the subendothelium of a damaged blood vessel is the initial step in formation of a haemostatic plug. (
  • It measures platelet aggregation with the help of von Willebrand factor (vWF) and exogenous antibiotic ristocetin added in a graded fashion. (
  • 6 PRP-platelet concentrates were subjected to adhesion analysis on collagen matrix under mild stirring condition as well as collagen-induced aggregation on day 1, 3 and 5 post-storage. (
  • Podoplanin expression by primary brain tumors induces platelet aggregation and is associated with hypercoagulability and a high risk of VTE. (
  • We found that ATP induces platelet aggregation in whole blood but not in PRP, and we have investigated the mechanisms that are involved. (
  • L-arginine infusion decreases peripheral arterial resistance and inhibits platelet aggregation in healthy subjects. (
  • In recent years, it has been shown that platelets are not only involved in the arterial thrombotic process, but also that they play an active role in the inflammatory process of atherogenesis from the beginning. (
  • Shear stress-induced platelet aggregation (SIPA), which occurs under abnormally high shear stress, plays a crucial role in the development of arterial thrombotic diseases. (
  • Studies on the mechanism of ristocetin-induced platelet adhesion. (
  • Generation of PGX by vessel walls could be the biochemical mechanism underlying their unique ability to resist platelet adhesion. (
  • Characterization of distinct mechanism of agonist-induced canine platelet activation. (
  • The effect and mechanism of action on veins, arteries, and platelets are not fully understood. (
  • Thus, the overall aim of this thesis was to investigate the possible mechanism(s) by which vanilloids inhibit platelet aggregation, both individually and in combination. (