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 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.
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.
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 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.
Glands that secrete SALIVA in the MOUTH. There are three pairs of salivary glands (PAROTID GLAND; SUBLINGUAL GLAND; SUBMANDIBULAR GLAND).
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
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.
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.
An acid dye used in testing for hydrochloric acid in gastric contents. It is also used histologically to test for AMYLOIDOSIS.
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.
Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.
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.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
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.
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.
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 3.6.1.5.
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.
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 5.3.99.5.
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.

Interleukin-12 is synthesized by mesangial cells and stimulates platelet-activating factor synthesis, cytoskeletal reorganization, and cell shape change. (1/4442)

Preliminary studies indicate the involvement of interleukin (IL)-12 in experimental renal pathology. In the present study, we evaluated whether cultured glomerular mesangial cells are able to produce IL-12 and whether IL-12 may regulate some of their functions, including the cytoskeletal reorganization, the change in cell shape, and the production of platelet-activating factor (PAF). The results obtained indicate that pro-inflammatory stimuli, such as tumor necrosis factor-alpha and bacterial polysaccharides, induce the expression of IL-12 mRNA and the synthesis of the protein by cultured mesangial cells. Moreover, cultured mesangial cells were shown to bind IL-12 and to express the human low-affinity IL-12 beta1-chain receptor. When challenged with IL-12, mesangial cells produced PAF in a dose- and time-dependent manner and superoxide anions. No production of tumor necrosis factor-alpha and IL-8 was observed. Moreover, we demonstrate that IL-12 induced a delayed and sustained shape change of mesangial cells that reached its maximum between 90 and 120 minutes of incubation. The changes in cell shape occurred concomitantly with cytoskeletal rearrangements and may be consistent with cell contraction. As IL-12-dependent shape change of mesangial cells was concomitant with the synthesis of PAF, which is known to promote mesangial cell contraction, we investigated the role of PAF using two chemically different PAF receptor antagonists. Both antagonists inhibited almost completely the cell shape change induced by IL-12, whereas they were ineffective on angiotensin-II-induced cell shape change. In conclusion, our results suggest that mesangial cells can either produce IL-12 or be stimulated by this cytokine to synthesize PAF and to undergo shape changes compatible with cell contraction.  (+info)

The mechanism of the increasing action of TA-993, a new 1,5- benzothiazepine derivative, on limb blood flow in anesthetized dogs: selective suppression of sympathetic nerve activity. (2/4442)

TA-993, (-)-cis-3-acetoxy-5-(2-(dimethylamino)ethyl)-2, 3-di-hydro-8-methyl-2-(4-methylphenyl)-1,5-benzothiazepin-4(5H)one maleate, a new 1,5-benzothiazepine derivative with l-cis configuration, has a unique and selective increasing action on limb blood flow with little influence on arterial pressure besides an antiplatelet action. We studied the mechanism of increasing action of TA-993 on limb blood flow in anesthetized dogs. In a canine blood-perfused hindlimb preparation with a donor dog, TA-993 (100 microg/kg i.v.) did not increase femoral blood flow when administered to the donor dog, but did when administered to a recipient dog. TA-993 did not show the increasing action on femoral blood flow in the presence of hexamethonium or phentolamine, whereas it did in the presence of propranolol or atropine. TA-993 also showed a weak increasing effect on heart rate, which was inhibited by any one of these blockers. TA-993 (300 microg/kg i.v.) did not alter the phenylephrine (1-100 ng/kg i.a.)- or the talipexole (3-100 ng/kg i.a.)-induced increase in perfusion pressure in an autoperfused hindlimb. These results suggest that the increasing action of TA-993 on limb blood flow is mediated by the sympathetic nervous system but that the adrenergic receptors are not likely to be the central point of action of this new agent. There is a possibility that the mechanism of the increasing action on heart rate is different from that of its increasing action on limb blood flow.  (+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. (3/4442)

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)

Glutamate receptor signaling interplay modulates stress-sensitive mitogen-activated protein kinases and neuronal cell death. (4/4442)

Glutamate receptors modulate multiple signaling pathways, several of which involve mitogen-activated protein (MAP) kinases, with subsequent physiological or pathological consequences. Here we report that stimulation of the N-methyl-D-aspartate (NMDA) receptor, using platelet-activating factor (PAF) as a messenger, activates MAP kinases, including c-Jun NH2-terminal kinase, p38, and extracellular signal-regulated kinase, in primary cultures of hippocampal neurons. Activation of the metabotropic glutamate receptor (mGluR) blocks this NMDA-signaling through PAF and MAP kinases, and the resultant cell death. Recombinant PAF-acetylhydrolase degrades PAF generated by NMDA-receptor activation; the hetrazepine BN50730 (an intracellular PAF receptor antagonist) also inhibits both NMDA-stimulated MAP kinases and neuronal cell death. The finding that the NMDA receptor-PAF-MAP kinase signaling pathway is attenuated by mGluR activation highlights the exquisite interplay between glutamate receptors in the decision making process between neuronal survival and death.  (+info)

Effects of docosahexaenoic and eicosapentaenoic acid on lipid metabolism, eicosanoid production, platelet aggregation and atherosclerosis in hypercholesterolemic rats. (5/4442)

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)

Predominant inhibition of ganodermic acid S on the thromboxane A2-dependent pathway in human platelets response to collagen. (6/4442)

Ganodermic acid S (GAS), a membrane acting agent, exerts multiple effects on human platelet function (C.N. Wang et al. (1991) Biochem. J. 277, 189-197). The study reported how GAS affected the response of human gel-filtered platelets (GFP) to collagen. The agent inhibited cell aggregation by prolonging lag and shape change periods and decreasing the initial cell aggregation rate. However, the inhibitory efficiency was less than its inhibition on GFP response to U46619, a thromboxane (TX) A2 mimetic. In the agent-effect on biochemical events, GAS effectively inhibited Ca2+ mobilization, phosphorylation of myosin light chain, dense granule secretion and TXB2 generation. The inhibitions might originate from blocking Ca2+ mobilization of the TXA2-dependent pathway. GAS partially decreased the phosphorylation of most phosphotyrosine proteins from early activation to the integrin alphaIIbbeta3-regulated steps. The agent did not affect the phosphorylation of three proteins at the steps regulated by integrin alphaIIbbeta3. The results suggest that GAS inhibits the collagen response predominantly on the TXA2-dependent signaling, and the tyrosine kinase-dependent pathway in collagen response plays a major role in aggregation.  (+info)

PAF binding to a single receptor in corneal epithelium plasma membrane. (7/4442)

PURPOSE: To study the binding characteristics and the expression of platelet-activating factor receptors (PAF-R) in corneal epithelium to elucidate the site of action of PAF. METHODS: Binding of [3H]PAF was investigated in subcellular fractions of the epithelia of bovine corneas and in membranes from cultured rabbit corneal epithelial cells. Dose-response inhibition curves of [3H]PAF-specific binding were generated using increasing concentrations of several PAF-R antagonists. RNA from rabbit corneal epithelial cells was probed for PAF-R expression by reverse transcription-polymerase chain reaction (RT-PCR) with specifically designed degenerated primers. RESULTS: Scatchard analysis showed a high-affinity binding site in bovine and rabbit corneal epithelium. The dissociation constant (Kd) and the maximum binding sites (Bmax) in a bovine membrane preparation and similar rabbit fraction were 0.77+/-0.03 nM and 180+/-21 femtomoles/mg protein and 4.3 nM and 1.3 picomoles/mg protein, respectively. Specific PAF-binding sites were found in bovine preparations enriched in plasma membranes with a Kd = 69.6 pM and Bmax = 80 femtomoles/mg protein; no specific binding was found in nuclei or microsomal fractions. RT-PCR of rabbit corneal epithelium generated a single product of the predicted size (478 bp). The deduced amino acid sequence of the purified PCR product was 87% homologous to human PAF-R. The hetrazepines BN 50727 and BN 50730 and the PAF structural analogues CV 3988 and CV 6209 competitively inhibited [3H]PAF binding to corneal epithelium with similar potency. WEB 2086 BS was two orders of magnitude less active in antagonizing PAF binding. CONCLUSIONS: Corneal epithelium contains a single population of receptors localized in the plasma membrane. PAF antagonists exert their actions by blocking this PAF-R. The partial sequence deduced in rabbit corneal PAF-R show a higher homology to the human PAF-R.  (+info)

Conformational changes in the A3 domain of von Willebrand factor modulate the interaction of the A1 domain with platelet glycoprotein Ib. (8/4442)

Bitiscetin has recently been shown to induce von Willebrand factor (vWF)-dependent aggregation of fixed platelets (Hamako J, et al, Biochem Biophys Res Commun 226:273, 1996). We have purified bitiscetin from Bitis arietans venom and investigated the mechanism whereby it promotes a form of vWF that is reactive with platelets. In the presence of bitiscetin, vWF binds to platelets in a dose-dependent and saturable manner. The binding of vWF to platelets involves glycoprotein (GP) Ib because it was totally blocked by monoclonal antibody (MoAb) 6D1 directed towards the vWF-binding site of GPIb. The binding also involves the GPIb-binding site of vWF located on the A1 domain because it was inhibited by MoAb to vWF whose epitopes are within this domain and that block binding of vWF to platelets induced by ristocetin or botrocetin. However, in contrast to ristocetin or botrocetin, the binding site of bitiscetin does not reside within the A1 domain but within the A3 domain of vWF. Thus, among a series of vWF fragments, 125I-bitiscetin only binds to those that overlap the A3 domain, ie, SpIII (amino acid [aa] 1-1365), SpI (aa 911-1365), and rvWF-A3 domain (aa 920-1111). It does not bind to SpII corresponding to the C-terminal part of vWF subunit (aa 1366-2050) nor to the 39/34/kD dispase species (aa 480-718) or T116 (aa 449-728) overlapping the A1 domain. In addition, bitiscetin that does not bind to DeltaA3-rvWF (deleted between aa 910-1113) has no binding site ouside the A3 domain. The localization of the binding site of bitiscetin within the A3 domain was further supported by showing that MoAb to vWF, which are specific for this domain and block the interaction between vWF and collagen, are potent inhibitors of the binding of bitiscetin to vWF and consequently of the bitiscetin-induced binding of vWF to platelets. Thus, our data support the hypothesis that an interaction between the A1 and A3 domains exists that may play a role in the function of vWF by regulating the ability of the A1 domain to bind to platelet GPIb.  (+info)

In SPS3 Trial dual anti-platelet therapy compared to aspirin alone exhibited no benefit and significant evidence of harm including risk of hemorrhage of 2.1% for dual anti-platelet therapy compared to 1.1% for aspirin alone and the dual anti-platelet therapy group also showed higher rates of mortality
The REPLACE-2 trial validated bivalirudin plus provisional GP IIb/IIIa blockade as an alternative anticoagulant regimen to heparin plus planned GP IIb/IIIa blockade during urgent or elective PCI. This substudy of the REPLACE-2 trial focused on the role of clopidogrel pretreatment with both these treatment strategies. Although administration of clopidogrel before PCI was associated with a trend toward lower rates of periprocedural ischemic events for patients who received either bivalirudin or heparin plus GP IIb/IIIa blockade, bivalirudin with provisional GP IIb/IIIa blockade was noninferior to heparin plus planned GP IIb/IIIa blockade in all subgroups irrespective of pretreatment or the duration of pretreatment. Moreover, there was no evidence that clopidogrel pretreatment attenuated the reduction in bleeding complications by bivalirudin. Therefore, clopidogrel pretreatment appears to improve clinical outcomes without compromising safety, but is not required for bivalirudin to achieve efficacy ...
Recently, several newer antiplatelet treatment strategies have been used in patients with coronary artery disease (CAD). Apart from the dual antiplatelet therapy (DAPT) consisting of aspirin and clopidogrel, double dose clopidogrel (DDC), triple antiplatelet therapy (TAPT) consisting of aspirin, clopidogrel and cilostazol and other newer antiplatelet agents have shown to be effective in different ways. In this analysis, we aimed to systematically compare the adverse clinical outcomes and the bleeding events which were observed when DDC was compared to the other antiplatelet regimens in patients with CAD. English publications comparing DDC with other antiplatelet regimens were searched from MEDLARS/MEDLINE, EMBASE, www.ClinicalTrials.gov and Google Scholar. Adverse cardiovascular outcomes and bleeding events were the study endpoints. Statistical analysis was carried out by the RevMan 5.3 software whereby odds ratios (OR) with 95% confidence
To the Editor:. We read with interest the work by Chen et al,1 which reported that triple antiplatelet therapy seems to be superior to dual antiplatelet therapy in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention with drug-eluting stents. Chen et al1 reported the mortality benefits of triple antiplatelet therapy obtained mainly within 30 days after STEMI, reflecting the importance of the addition of cilostazol to aspirin and clopidogrel before stenting. Meanwhile, the authors pointed out the limitation of the nonrandomized trial, that several baseline differences were present between the groups. In our opinion, the advantage of the short-term outcome of triple therapy should be emphasized in higher-risk patients with STEMI undergoing primary percutaneous coronary intervention regardless of whether cilostazol or abciximab was selected.. Because glycoprotein IIb/IIIa inhibitors (abciximab) as adjunctive pharmacological therapy ...
DAPT - Dual Antiplatelet Therapy. Looking for abbreviations of DAPT? It is Dual Antiplatelet Therapy. Dual Antiplatelet Therapy listed as DAPT
Background: The potential benefits and risks of the use of dual anti-platelet therapy (DAT) beyond 12 months in patients receiving drug-eluting stents (DES) with acute myocardial infarction (AMI) have not been clearly established.. Methods: We analyzed 795 patients who had undergone DES implantation with AMI and had been free of major adverse cardiac or cerebrovascular events at least for 12 months in prospective multi-center registry (Infarct Prognosis Study). The duration of DAT was categorized in group 1 (N=185): ≤ 12 months and group 2 (N=610): , 12 months. The incidence of cardiac death or recurrent MI was compared between 2 groups.. Results: The median duration of follow up was 28.4 months. The Kaplan Meier analysis indicated a benefit of group 2 compared with less than group 1. (2.5 % vs. 8.6 %, log rank test p , 0.001). Continuation of DAT beyond 12 months showed the significant reduction of cardiac death or recurrent MI in Cox proportional hazards analysis even after controlling of ...
Dual anti-platelet therapy following percutaneous coronary intervention (PCI) for the treatment of STEMI has traditionally consisted of aspirin and clopidogrel. Despite this treatment approach, a substantial portion of patients experience recurrent adverse cardiovascular events including death, myocardial infarction, and stent thrombosis. This persistent vulnerability has been associated with inadequate platelet inhibition in response to clopidogrel administration, a phenomenon referred to as high on-treatment platelet reactivity. Although multiple variables have been implicated in altered clopidogrel response, mounting evidence has suggested a crucial role for common genetic variants including: CYP2C19*2, *17, and ABCB1 3435 C,T alleles.. Presence of the CYP2C19*2 allele has been associated with a 1.5- to 6-fold increased risk of cardiovascular death, myocardial infarction, and stent thrombosis following PCI in patients treated with clopidogrel. These findings, recently bolstered by 2 separate ...
Participating Centers : 38 french high PCI volume (,700) centers Rationale: Clopidogrel / Prasugrel (75 mg/day), in combination with aspirin (75 mg/day), is currently the antiplatelet treatment of choice for prevention of stent thrombosis, and clinical trials have shown that, in high-risk patients, prolonged dual antiplatelet treatment is more effective than aspirin alone in preventing major cardiovascular events. However, despite the use of clopidogrel, a considerable number of patients continue to have cardiovascular events. Numerous in VITRO studies have shown that individual responsiveness to clopidogrel but also to aspirin is not uniform in all patients and is subject to inter- and intraindividual variability. The recent possibility of bedside monitoring of oral antiplatelet therapy offers the unique opportunity of tailoring antiplatelet therapy. However, the relevance of such strategy has never been evaluated in a randomized prospective adequately powered study having long term follow-up ...
A one-month treatment of dual anti-platelet therapy is safe and as effective as a longer duration of therapy at preventing cardiac events in patients one year after stent placement, according to late-breaking research presented today at the American Heart Associations Scientific Sessions 2020.
TY - JOUR. T1 - Optimal duration of dual antiplatelet therapy after drug-eluting stent implantation a randomized, controlled trial. AU - Lee, Cheol Whan. AU - Ahn, Jung Min. AU - Park, Duk Woo. AU - Kang, Soo Jin. AU - Lee, Seung Whan. AU - Kim, Young Hak. AU - Park, Seong Wook. AU - Han, Seungbong. AU - Lee, Sang Gon. AU - Seong, In Whan. AU - Rha, Seung Woon. AU - Jeong, Myung Ho. AU - Lim, Do Sun. AU - Yoon, Jung Han. AU - Hur, Seung Ho. AU - Choi, Yun Seok. AU - Yang, Joo Young. AU - Lee, Nae Hee. AU - Kim, Hyun Sook. AU - Lee, Bong Ki. AU - Kim, Kee Sik. AU - Lee, Seung Uk. AU - Chae, Jei Keon. AU - Cheong, Sang Sig. AU - Suh, Il Woo. AU - Park, Hun Sik. AU - Nah, Deuk Young. AU - Jeon, Doo Soo. AU - Seung, Ki Bae. AU - Lee, Keun. AU - Jang, Jae Sik. AU - Park, Seung Jung. PY - 2014/1/21. Y1 - 2014/1/21. N2 - Background-The risks and benefits of long-term dual antiplatelet therapy remain unclear. Methods and Results-This prospective, multicenter, open-label, randomized comparison trial was ...
OBJECTIVE: To determine the effects of antiplatelet therapy among patients at high risk of occlusive vascular events. DESIGN: Collaborative meta-analyses (systematic overviews). INCLUSION CRITERIA: Randomised trials of an antiplatelet regimen versus control or of one antiplatelet regimen versus another in high risk patients (with acute or previous vascular disease or some other predisposing condition) from which results were available before September 1997. Trials had to use a method of randomisation that precluded prior knowledge of the next treatment to be allocated and comparisons had to be unconfounded-that is, have study groups that differed only in terms of antiplatelet regimen. STUDIES REVIEWED: 287 studies involving 135 000 patients in comparisons of antiplatelet therapy versus control and 77 000 in comparisons of different antiplatelet regimens. MAIN OUTCOME MEASURE: Serious vascular event: non-fatal myocardial infarction, non-fatal stroke, or vascular death. RESULTS: Overall, among these
We investigated the impact of suboptimal platelet reactivity on clinical outcomes after percutaneous coronary intervention (PCI). We enrolled 500 patients with stable coronary artery disease...
To help prevent this, physicians may prescribe antiplatelets in patients who are at high risk for developing a thrombus within their blood vessels. Antiplatelets are types of anticoagulants - medications used to help prevent the formation of blood clots when no injury has occurred. They work by reducing the platelets stickiness (viscosity). The most common antiplatelet in use today is the over-the-counter drug aspirin, which has been found to prevent platelet binding and clot formation. Today, many physicians place their heart patients on a small daily dose of aspirin (generally 81 milligrams) to prevent the formation of blood clots that may injure the heart. For patients who do not respond to aspirin as a preventive therapy, other antiplatelet medications are available. The most common are clopidogrel and ticlopidine ...
[Percutaneous coronary intervention (PCI) is meant to optimalise cardiac status, that is, short-term and long-term outcomes. It is known from large Western databases that stent implantation is performed in 77-85% of coronary interventions, which means hundreds of thousands of new patients with stent every year. The great majority of these patients has to take platelet aggregation inhibitors, namely acetylsalicylic acid and thienopyridin, most often clopidrogel. It presents a major therapeutic dilemma when these patients require noncardiac surgery. First, surgery should be performed with the least possible blood loss, which would be optimal if the platelet aggregation inhibitor therapy - that is indispensable for a certain period because of the stent - was suspended. Second, stent thrombosis has to be avoided, which can only be achieved if platelet aggregation inhibitor therapy is continued. The aim of our paper is to summarise the current guidelines and the risk estimation on the basis of our current
We read with interest the CILON-T (Influence of Cilostazol-based Triple Antiplatelet Therapy on Ischemic Complication After Drug-Eluting Stent Implantation) trial on the efficacy of cilostazol on ischemic complications after drug-eluting stent (DES) implantation (1), which suggested the potential link between platelet reactivity and ischemic events in Asians.. Asians exhibit poor response to clopidogrel, maybe due to the high prevalence of CYP2C19*2/*3 allele carriage (∼55% to 70%) (1). In the CILON-T study, ,50% of the patients receiving dual antiplatelet therapy had high platelet reactivity based on Western population (P2Y12 reaction units [PRU] ,235). However, similar to other Asian studies, the CILON-T study showed a low ischemic events rate (∼2% during 6 months). In the CILON-T study, patients under the certain PRU (,210) were absent from ischemic events (1). Meanwhile, the GRAVITAS trial demonstrated a different threshold (∼175 PRU), showing the complete immunity against 6-month ...
Prolonging dual antiplatelet therapy with aspirin plus clopidogrel (Plavix) for more than one year after the placement of a drug-eluting stent confers no clinical benefit.
IMPORTANCE: Dual antiplatelet therapy after percutaneous coronary intervention (PCI) reduces ischemia but increases bleeding.. OBJECTIVE: To develop a clinical decision tool to identify patients expected to derive benefit vs harm from continuing thienopyridine beyond 1 year after PCI.. DESIGN, SETTING, AND PARTICIPANTS: Among 11,648 randomized DAPT Study patients from 11 countries (August 2009-May 2014), a prediction rule was derived stratifying patients into groups to distinguish ischemic and bleeding risk 12 to 30 months after PCI. Validation was internal via bootstrap resampling and external among 8136 patients from 36 countries randomized in the PROTECT trial (June 2007-July 2014).. EXPOSURES: Twelve months of open-label thienopyridine plus aspirin, then randomized to 18 months of continued thienopyridine plus aspirin vs placebo plus aspirin.. MAIN OUTCOMES AND MEASURES: Ischemia (myocardial infarction or stent thrombosis) and bleeding (moderate or severe) 12 to 30 months after ...
To the Editor:. We read with great interest the recent article published by Fiorella et al who report a multicenter experience with the use of the Wingspan stent system (Boston Scientific) for the treatment of intracranial atherosclerosis.1 This collaborative effort should be applauded, but we would advocate for closer scrutiny to future registry designs in order to enhance our understanding of treatment modalities being used.. A total of 78 patients with 82 lesions were treated with a high technical success rate and a periprocedural complication rate (stroke or death) of 6.1%.1 We would like to bring attention to 3 issues that may help with further study in this area. The first is the patient selection for the registry. Nineteen of the 78 (24%) patients were not on antiplatelet therapy at the time of their stroke or transient ischemic attack. The natural history of patients who were not on antiplatelet therapy is not clear to date; thus, selection of such patients for angioplasty and stenting ...
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Arguably, antiplatelet agents are the most important therapy we administer to stented patients. Antiplatelet agents are given to prevent the most dreaded event that often has catastrophic consequences, coronary thrombosis. It is well established that platelet reactivity to adenosine diphosphate (ADP) mediated by the P2Y12 receptor plays a central role in the development of post-percutaneous coronary intervention (PCI) ischemic events, including stent thrombosis. The active metabolite of clopidogrel blocks this pivotal receptor (1,2). Platelet reactivity to ADP during clopidogrel therapy has been determined by turbidimetric aggregometry, VerifyNow (Accumetrics, San Diego, California) assay, Thrombelastography (TEG, Hemonetics, Braintree, Massachusetts), Multiplate Analyzer (Dynabyte Informationssysteme GmbH, Munich, Germany), and flow cytometry to measure phosphorylated vasodilator stimulated phosphoprotein (VASP Assay, Biocytex, Marseille, France). All of these methods have demonstrated ...
Dual antiplatelet therapy (DAPT) with acetylsalicylic acid and an inhibitor of the adenosine diphosphate platelet receptor P2Y12 has been shown to reduce the risk of stent thrombosis (ST), myocardial infarction and cardiac death after percutaneous coronary intervention (PCI) with bare-metal stents (BMS) and drug-eluting stents (DES). However, while there is consensus on 1-month DAPT after BMS, the optimal duration and the risk-benefit ratio of DAPT duration after DES implantation remains controversial. Controversy surrounding this issue is demonstrated by differences in guideline recommendations for DAPT duration after PCI with DES. For example, while the ACC/AHA recommends a minimum of 12 months, ESC guidelines recommend at least 6 months of DAPT. Recent reports suggest that 6 months of DAPT after second-generation DES implantation might be safe compared with longer durations. Large randomized controlled trials powered to examine ST and bleeding events are currently ongoing and will shed novel ...
CO Clopidogrel: Clopidogrel belongs to the class of medications called platelet aggregation inhibitors or antiplatelets. Clopidogrel is used to help prevent heart attacks, strokes, and other circulation problems in people who have atherosclerosis (narrowed blood vessels caused by hardening of the arteries) and have already experienced at least one atherothrombotic event such as heart attack, stroke, or diagnosed peripheral arterial disease (problems with blood flow in the arteries). It is also used with ASA (acetylsalicylic acid) by people with acute coronary syndrome or atrial fibrillation (a fast, irregular heartbeat).
In patients with ACS (NSTE-ACS or STEMI) treated with coronary stent implantation who have tolerated DAPT without a bleeding complication and who are not at high bleeding risk (e.g., prior bleeding on DAPT, coagulopathy, oral anticoagulant use), continuation of DAPT (clopidogrel, prasugrel, or ticagrelor) for longer than 12 months may be reasonable (Class IIb). A new risk score (the DAPT score), derived from the Dual Antiplatelet Therapy study, may be useful for decisions about whether to continue (prolong or extend) DAPT in patients treated with coronary stent implantation ...
Part I Concepts in Platelet Physiology, Function and Measurement. 1 Platelet physiology and the role of the platelet in ischemic heart disease.. Robert F. Storey .. 2 Laboratory assessment of platelet function and the effects of antiplatelet agents.. Alan D. Michelson, A.L. Frelinger .. Part II Pharmacology of Oral Antiplatelet Agents.. 3 Cyclooxygenase inhibitors.. Nina Chetty Raju, John W. Eikelboom .. 4 Aspirin response variability and resistance.. Wai-Hong Chen, Daniel I. Simon .. 5 P2Y12 inhibitors: Thienopyridines and direct oral inhibitors.. Jean-Philippe Collet, Boris Aleil, Christian Gachet, Gilles Montalescot .. 6 Thienopyridine response variability and resistance.. Udaya S. Tantry, Thomas A. Suarez, Paul A. Gurbel .. Part III Pharmacology of Intravenous Antiplatelet Agents.. 7 Pharmacology of intravenous glycoprotein IIb/IIIa antagonists.. James C. Blankenship, Peter B. Berger .. 8 Intravenous P2Y12 inhibitors.. Steven P. Dunn, Steven R. Steinhubl .. 9 Antiplatelet effects of thrombin ...
There are limited real-world data on prevalence and predictors of dual antiplatelet therapy (DAPT) prolongation beyond one year after acute coronary syndrome (ACS). We have explored such issue in the START ANTIPLATELET Registry, which is a prospective, observational, multicenter, Italian registry performed in seven Italian cardiology institutions including patients admitted for ACS and followed up to one year. Out of a total population of 840 ACS patients, 596 patients had completed 12-month follow-up being on DAPT. Decision to prolong DAPT beyond one year was taken in 79 patients (13%), whereas in 517 patients DAPT was stopped. The strongest predictors of DAPT continuation were a new cardiovascular events after the index admission event (OR 3.3, 95% CI 1.4-7.7), no bleeding complications (OR 3.2, 95% CI 1.2-8.3) and no anemia during one-year follow-up (OR 2.6, 95% CI 1.1-5.9); other independent predictors were renal failure (OR 2.5, 95% CI 1.3-5.0) and peripheral artery disease (OR 1.8, 95% CI ...
Journal cover image about duration of dual anti platelet therapy following angioplasty. Antiplatelet medicines work to keep platelets from sticking together and forming blood clots. There have been many recent studies debating whether shorter or longer courses of dual antiplatelet therapy are better for patients undergoing percutaneous coronary intervention.
Title:Antiplatelet Therapy in Children: Why So Different from Adults?. VOLUME: 18 ISSUE: 21. Author(s):Pier Paolo Bassareo, Vassilios Fanos, Nicoletta Iacovidou and Giuseppe Mercuro. Affiliation:Department of Cardiovascular and Neurological Sciences, University of Cagliari, Policlinico Universitario, S.S. 554, bivio di Sestu -09042 Monserrato (Cagliari).. Keywords:Platelet, antiplatelet agents, aspirin, haemostasis, paediatric, coronary heart disease, ischemic stroke, peripheral arterial disease, arrhythmias, thromboembolic complications. Abstract:Antiplatelet agents are administered in the treatment of a large number of adult diseases: coronary heart disease, ischemic stroke, peripheral arterial disease, arrhythmias with their thromboembolic complications, primary and secondary prevention. In childhood however, the situation is substantially different. The lack of large interventional trials on the use of antiplatelet drugs in children, has led to greater uncertainty, and a less extensive use ...
People with peripheral vascular disease are at high risk of vascular events and major adverse limb events. Use of antiplatelet therapy is effective at reducing this risk. Other antithrombotic strategies that have been tested, such as use of anticoagulation, dual antiplatelet therapy or novel antiplatelet agents, have not been found to be superior to single antiplatelet therapy. The new oral factor Xa inhibitors such as rivaroxaban have been shown to be at least as effective as vitamin K antagonists in preventing thromboembolic events in atrial fibrillation,1 and offer a potential alternative strategy, either in addition to, or instead of, a single antiplatelet agent. ...
Clopidogrel has anti-platelet activity by irreversible inhibition of the P2Y12 platelet receptor. Clopidogrel must be converted into an active metabolite in order to show anti-platelet activity. Hepatic CYP2C19 enzyme is one of the key hepatic enzymes which convert clopidogrel into active metabolite and its genetic polymorphism is related to clopidogrel resistance. CYP2C19 poor or intermediate metabolizer groups show reduced anti-platelet activity of clopidogrel compared to extensive metabolizer group ...
Health, ...The findings were presented by Dr Jolanta Siller-Matula from Medical U...Standard antiplatelet treatment in patients undergoing percutaneous co...But measurements of platelet aggregation in clopidogrel treated patien...Personalized antiplatelet treatment involves choosing a therapy base...,Personalized,antiplatelet,treatment,improves,outcome,after,PCI,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
Objective We retrospectively assessed the incidence of hemorrhagic complications associated with pacemaker implantation in patients receiving one or more antiplatelet agents.
Three year follow-up of patients who received dual antiplatelet therapy (DAPT) after placement of a drug-eluting stent (DES) shows that a short course of the therapy continues to be as beneficial as a longer course.
Clopidogrel belongs to the class of medications called platelet aggregation inhibitors or antiplatelets. Clopidogrel is used to help prevent heart attacks, strokes, and other circulation problems in people who have atherosclerosis (narrowed blood vessels caused by
Novel oral anti-coagulants (NOACs) are increasingly being used in clinical practice and are set to almost entirely replace the vitamin K antagonists, such as warfarin, in the near future. Similarly, new antiplatelet agents are now regularly used in place of older agents, such as aspirin and clopidogrel. In an ageing population, with an increasing burden of complex comorbidities, urologists will frequently encounter patients who will be using such agents. Some background knowledge, and an understanding, of these drugs and the issues that surround their usage, is essential. The present article will provide readers with an understanding of these new drugs, including their mechanisms of action, the up-to-date evidence justifying their recent introduction into clinical practice and the appropriate interval for stopping them before surgery. It will also consider the risks of perioperative bleeding for patients taking these drugs and the risks of venous thromboembolism in those in whom they are ...
Antiplatelet agentsThese agents inhibit the cyclo-oxygenase system, decreasing the level of thromboxane A2, which is a potent platelet activator.Aspirin (Bayer Buffered Aspirin, Bayer Aspirin, Anacin)... more
Platelet adhesion, activation and aggregation to the injured vessel wall are crucially involved in the pathogenesis of thrombus formation. Agents in theory thwarting thes..
After coronary artery stenting, patients are maintained on dual antiplatelet therapy (DAPT). When presenting for elective surgery, these medications are often held to minimize bleeding risk intraoperatively. The ideal timeframe to wait after stenting before proceeding with elective surgery is guideline based, and therefore does change periodically. [More… ...
Dr. Routh responded: Different Actions. Anticoagulants are medicines which keep the blood from clotting by action on factors in the blood which are needed to stop bleeding. Oral examples would include |a href=/topics/warfarin track_data={
Riva-Clopidogrel: Clopidogrel belongs to the class of medications called platelet aggregation inhibitors or antiplatelets. Clopidogrel is used to help prevent heart attacks, strokes, and other circulation problems in people who have atherosclerosis (narrowed blood vessels caused by hardening of the arteries) and have already experienced at least one atherothrombotic event such as heart attack, stroke, or have been diagnosed peripheral arterial disease (problems with blood flow in the arteries). It is also used with ASA (acetylsalicylic acid) by people with acute coronary syndrome or atrial fibrillation (a fast, irregular heartbeat) to reduce the risk of heart attack or stroke.
Looking for online definition of Platelet aggregation inhibitor in the Medical Dictionary? Platelet aggregation inhibitor explanation free. What is Platelet aggregation inhibitor? Meaning of Platelet aggregation inhibitor medical term. What does Platelet aggregation inhibitor mean?
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Comparison of two platelet glycoprotein IIb/IIIa inhibitors, tirofiban and abciximab, for the prevention of ischemic events with percutaneous coronary revascularization
TY - JOUR. T1 - Safety issues surrounding use of platelet GP IIb/IIIa antagonists. T2 - Reversibility and readministration. AU - Kleiman, Neal. AU - Tcheng, J. E.. PY - 1999/1/1. Y1 - 1999/1/1. N2 - The platelet glycoprotein IIb/IIIa (GPIIb/IIIa) receptor antagonists abciximab, eptifibatide, and tirofiban have been shown to be safe and effective in patients with acute coronary syndromes and in those undergoing percutaneous coronary intervention. Consequently, the use of these drugs is becoming increasingly common. However, issues regarding the ability to reverse their effects remain, particularly in the setting of emergency surgery. The short-acting agents eptifibatide and tirofiban are characterized by less avid binding, significant plasma reservoirs of unbound drug, rapid decay of receptor occupancy and relatively rapid clearance in the presence of intact renal/hepatic mechnisms. The avid-binding abciximab is characterized by a shorter plasma half-life, relative absence of unbound drug, a long ...
TY - JOUR. T1 - Relationship between high platelet turnover and platelet function in high-risk patients with coronary artery disease on dual antiplatelet therapy. AU - Cesari, Francesca. AU - Marcucci, Rossella. AU - Caporale, Roberto. AU - Paniccia, Rita. AU - Romano, Eloisa. AU - Gensini, Gian Franco. AU - Abbate, Rosanna. AU - Gori, Anna Maria. PY - 2008/5. Y1 - 2008/5. N2 - A high platelet turnover rate produce a population of immature reticulated platelets (RP) that could confer, despite of antiplatelet drugs, a residual platelet reactivity (RPR) in coronary artery disease (CAD) patients. To assess the influence of RP on platelet reactivity in CAD patients on dual antiplatelet therapy we measured RP in 372 patients by using the Sysmex XE-2100 haematology analyzer and platelet function by optical platelet aggregometry (PA) on platelet-rich-plasma induced by 1 mmol arachidonic acid (AA-PA) and 10 μM ADP (ADP-PA). RPR was defined as either AA-PA ,20% or ADP-PA ,70%. RP were expressed as a ...
Inflammation plays an important role in plaque development and left ventricular remodeling during acute myocardial infarction (AMI). Clopidogrel may exhibit some anti-inflammatory properties and high loading dose of clopidogrel results in improved clinical outcomes in patients with AMI. 357 patients who received successful primary percutaneous coronary intervention from January 2008 to March 2011 in Peking University Third Hospital were included in this study. Different loading dose of clopidogrel (300 mg, 450 mg, or 600 mg) was given at the discretion of the clinician. Neutrophils reached their peak values on the first day after AMI. Higher levels of peak neutrophil and lower left ventricular ejection fraction (LVEF) were found in patients of low clopidogrel loading dose group (300 mg or 450 mg). After adjusting for the related confounders, a logistic regression model showed that low clopidogrel loading dose remained an independent predictor of low LVEF (LVEF ≤
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PPIs are widely prescribed in conjunction with antiplatelet therapy. Current American Heart Association guidelines recommend that all patients on dual antiplatelet therapy be prescribed a PPI regardless of Helicobacter pylori status or gastrointestinal bleeding risk.20 PPIs are inhibitors of CYP2C19 in vitro, with omeprazole showing more potent inhibition than newer-generation PPIs such as pantoprazole.21 Based on this evidence, several studies have assessed RPA in patients coprescribed clopidogrel and a PPI. For omeprazole, there is a significant increase in RPA in patients prescribed both clopidogrel and a PPI compared with clopidogrel alone.22 The results for other PPIs, particularly pantoprazole, are less clear. One study showed that RPA in ACS patients on clopidogrel and pantoprazole was similar to that of patients on clopidogrel alone,23 suggesting a compound-specific effect.. Despite the evidence that at least some PPIs affect residual platelet function in patients taking clopidogrel, the ...
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Aims: Antiplatelet therapy with aspirin and clopidogrel are recommended for 1 year after drug-eluting stent (DES) implantation or myocardial infarction. However, the discontinuation of antiplatelet therapy has become an important issue as recent studies have suggested a clustering of ischaemic events within 90 days of clopidogrel withdrawal. The objective of this investigation was to explore the hypothesis that there is a transient rebound increase in platelet reactivity within three months of clopidogrel discontinuation. Methods and Results: In this prospective study, platelet function was assessed in patients taking aspirin and clopidogrel for at least 1 year following DES implantation. Platelet aggregation was measured using a modification of light transmission aggregometry in response to multiple concentrations of adenosine diphosphate (ADP), epinephrine, arachidonic acid, thrombin receptor activating peptide and, collagen. Clopidogrel was stopped and platelet function was reassessed 1 week, 1
The findings provided in this report indicate that prevalence of prescribing aspirin or other antiplatelet medications at outpatient health-care visits is low for patients who have been recommended to receive these medications based on the presence of ischemic vascular disease or certain risk factors. Despite the low prevalence of aspirin prescribing identified in this analysis, other studies using the same data sources have demonstrated that aspirin and other antiplatelet medication prescribing among patients with ischemic vascular disease was only 32.8% in 2003 (16). Previous reports have estimated that for every 10% increase in the use of antiplatelet medication among eligible adults aged 18-79 years, an estimated 8,000 deaths per year would be prevented (21). A 2006 study that ranked clinical preventive services based on cost effectiveness and the clinically preventable burden of disease demonstrated that aspirin prevention counseling was one of three prevention services that received the ...
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Stenting and GP IIb/IIIa inhibition are promising adjunctive therapies in PCI. The Global Registry of Acute Coronary Events (GRACE) is a registry of unselected patients with acute coronary syndromes, allowing for the study of treatments in a real-world environment. Data from GRACE patients with AMI who underwent PCI were analyzed. After adjusting for demographics, baseline characteristics, and previous medications, treatment with GP IIb/IIIa inhibitors and a stent and treatment with a stent alone were significant predictors of survival at 6 months. Stents were used in 90.9% of patients. GP IIb/IIIa inhibitors were used in 59.7%; in most cases they were started after the beginning of the procedure. The in-hospital death rate (7.6%) was highest in patients undergoing urgent PCI. Mortality at 6 months following PCI was 14.4% among patients who received neither GP IIb/IIIa inhibitors nor a stent, compared to patients who received both GP IIb/IIIa inhibitors and a stent (7.3%), GP IIb/IIIa inhibitors alone
Current guidelines recommend aspirin, aspirin plus clopidogrel or aspirin plus extended-release dipyridamole for treatment of acute ischaemic stroke (IS) or transient ischaemic attack (TIA) to prevent recurrent stroke, myocardial infarction and cardiovascular death.1 The Clopidogrel in High-risk patients with Acute Non-disabling Cerebrovascular Events (CHANCE) trial randomised 5170 Chinese patients within 24 h after the onset of IS or TIA to clopidogrel plus aspirin versus aspirin plus placebo for 90 days. Clopidogrel plus … ...
This study found no significant benefit associated with clopidogrel continuation (use of clopidogrel plus aspirin) as compared with clopidogrel discontinuation (use of aspirin alone) after 6 months, in reducing the incidence of death from any cause, myocardial infarction, or cerebrovascular accident at 2 years. On the other hand, 2-year clopidogrel therapy resulted in a significant increase of actionable bleeding episodes, which included events requiring medical or surgical treatment, red blood cell transfusion, and life-threatening events. There seems to be little rationale for continuing dual antiplatelet therapy for more than a year after percutaneous coronary intervention, based on this and other available evidence.. ...
Over 1 million coronary stent procedures are performed annually in the U.S., with dual-antiplatelet therapy, which includes the use of both aspirin and clopidogrel, being a cornerstone in the management of these patients after coronary intervention. Now, recent data have surfaced demonstrating altered active metabolite levels of clopidogrel in patients harboring hepatic cytochrome gene variants. These variants, which have been validated through genome-wide association as the dominant explanation for the marked heterogeneity of clopidogrel response, are linked to a significant increase in the risk for bleeding, stent thrombosis, myocardial infarction, and death. With viable alternatives to clopidogrel now available, including higher clopidogrel maintenance and loading doses, prasugrel, and ticagrelor, clinicians can now effectively guide therapy in those with at-risk gene variants by simple genotyping. Such an individualized approach can potentially prevent tens of thousands of adverse cardiovascular
Platelet aggregation inhibitors, also known as antiplatelet therapy (APT), are prescribed for the prevention of secondary cardiovascular events (CVE) after endovascular revascularization procedures.- Platelet aggregation inhibitors are not equally effective in all patients. The phenomenon of high residual platelet reactivity despite APT is called high on-treatment platelet reactivity (HTPR); ... read more it bears an increased risk of secondary CVE.- Platelet function tests (PFT) can be used to diagnose HTPR. There are various tests available; of those, light transmission aggregometry (LTA) is considered the gold standard. Some tests are only suitable for determining the effect of a certain category of APT.- Research into the usefulness of PFTs to optimise treatment with APT has not yet produced an unambiguous conclusion.- Currently there is not yet an indication for routine use of PFT in clinical practice. However, for the treatment of certain categories of patients with thromboembolic ...
In this study of 64 294 patients undergoing PCI within the VA, the use of any contraindicated antiplatelet medications was associated with increased bleeding risk. Although the use of contraindicated medications was not significantly associated with risk-adjusted mortality, the point estimates suggested harm. Nearly 20% of patients undergoing PCI had a known contraindication to ≥1 antiplatelet medications, and ,1 in 20 of those patients received a contraindicated medication. In adjusted analyses, use of abciximab in patients with contraindications of thrombocytopenia or previous stroke likely increased the risk of major bleeding.. Although the overall rate of contraindicated mediation use among patients with PCI is low (1.1%), this study highlights the problem of medication errors in the United States. Importantly, these data illustrate that the use of contraindicated antiplatelet medications persist, despite high-profile reports and EMR built-in warnings.3 Medication errors are a major ...
The relationship between bleeding complications and increased mortality after percutaneous coronary intervention (PCI) has been well documented. Bivalirudin is superior to heparin and glycoprotein (GP) IIb/IIIa inhibitors, mainly due to the lower risk of bleeding but comparable rates of ischemic complications (1-3). Three trials presented at the 2014 American College of Cardiology Scientific Sessions raise questions regarding the superiority of bivalirudin in PCI (4-6).. In the HEAT-PPCI (Unfractionated Heparin Versus Bivalirudin in Primary Percutaneous Coronary Intervention) trial, 1,829 patients from a single center with ST-segment elevation myocardial infarction (STEMI) referred for primary PCI were randomized to heparin (70 U/kg bolus) or bivalirudin, with GP IIb/IIIa inhibitor only used for bail out (15.5% vs. 13.5%, p = NS) (4). The majority of the PCI (,80%) were performed transradially. Nearly all patients (99.6%) were pre-loaded with dual antiplatelet therapy; 60% of patients received ...
Keywords: platelet, IIIa antagonist, abciximab, eptifibatide, tirofiban, lamifiban, thrombocytopenia, angioplasty. Abstract: The activation of platelets and the resultant aggregation have been shown to play important role in the pathogenesis of cardiovascular, cerebrovascular and peripheral vascular diseases and in acute coronary syndromes. Hence platelet adhesion and aggregation have been identified as promising targets for the development of anti-thrombotic drugs. Glycoprotein (GP) IIb / IIIa antagonism exerts a strong anti-platelet effect, because this interference inhibits the final common pathway of platelet aggregation and is not dependent on a single activation pathway. Three GPIIb / IIIa antagonists have been approved by the US Food and Drug administration. They include abciximab (the chimeric monoclonal antibody 7E3 Fab fragment), eptifibatide (the cyclic heptapeptide based on the KGD amino acid sequence) and tirofiban (a nonpeptide tyrosine derivative). In addition, nonpeptide oral ...
High residual platelet reactivity (HRPR) on clopidogrel treatement is associated with an increased risk of adverse events after percutaneous coronary intervention (PCI) and the three REsponsiveness to CLopidogrel and Stent Thrombosis (RECLOSE) studies showed this relationship, the futility of a tailored therapy with increasing dose of clopidogrel, and that nonresponsiveness to clopidogrel is a modifiable risk factor.. RECLOSE-1 1,2. This study is based on a cohort of of 804 patients who had successful sirolimus- or paclitaxel-eluting stent implantation. All patients received a loading dose of 600 mg of clopidogrel, and residual platelet reactivity was assessed by light transmittance aggregometry (LAT) using 10 µmol of adenosine diphosphate as agonist. Patients with platelet aggregation by 10 µmol ADP ≥70% were defined as nonresponders. All patients received chronic dual antiplatelet treatment (aspirin 325 mg and clopidogrel 75 mg daily) for 6 months. The primary end point was the incidence ...
Initial platelet activity may predict efficacy after chronic oral glycoprotein IIb/IIIa blockade: should we still consider uniform treatment regimens?
Eptifibatide, a platelet glycoprotein IIb/IIIa inhibitor substantially reduces ischemic complications in coronary stent interventions and could become a routine pre-treatment in stent coronary implantation, concludes a study published in 16 December Lancet (Lancet 2000 356:2037).In a prospective study, Dr James Tcheng and colleagues from Duke University Medical Centre in North Carolina recruited 2064 patients who were undergoing coronary stent implantation. Immediately before the procedure, pati
Bristol-Myers Squibb (NYSE: BMY) is no longer offering its $37-a-month Plavix® Co-Pay Discount Card. And some patients are not happy about this. Additionally, according to the companys web site for Patient Assistance Programs, the company is no longer making this life-saving drug available to patients who cannot afford it. This, of course, has something to do with the fact that brand-name Plavix has gone off patent and generic versions have been available since May 2012. (See our Patient Alert: How to Get the Best Price on New Generic Plavix.) But are the generic versions of clopidogrel really the same?. Plavix (clopidogrel) is a critical component of all drug-eluting stent implantations. One year of Dual AntiPlatelet Therapy or DAPT (aspirin plus clopidogrel or prasugrel or ticagrelor or even the older ticlopidine) is a package deal with drug-eluting stents: you cant have one without the other. Thats why Financial Assistance for Plavix has been one of the most popular topics in ...
The central role played by the alphaIIb beta3 receptor in platelet aggregation, and hence in platelet thrombosis, has led to the development of a number of parenteral and oral glycoprotein (GP) IIb/IIIa inhibitors for use in cardiovascular disease states, such as acute coronary syndromes and stroke. The predominant effect of these agents is to inhibit platelet aggregation, although studies of alphaIIb beta3 receptor function and various GP IIb/IIIa inhibitors have demonstrated the potential for these agents to produce effects on other aspects of platelet function, in addition to non-platelet effects. Overall, clinical studies have demonstrated an impressive beneficial effect for parenteral agents in reducing ischemic complications following percutaneous intervention, and a more modest beneficial effect in the treatment of patients with acute coronary syndromes. Trials with oral GP IIb/IIIa inhibitors in similar patient populations have demonstrated toxicity, manifested by an increased mortality ...
The study sought to evaluate the presence of a clinically relevant rebound phenomenon after dual antiplatelet therapy discontinuation in randomized trials.
Clinical and economic studies of eptifibatide in coronary stenting Tilak Pasala, Prasongchai Sattayaprasert, Pradeep K Bhat, Ganesh Athappan, Sanjay Gandhi The Heart and Vascular Center, Case Western Reserve University/MetroHealth, Cleveland, OH, USA Abstract: Platelet adhesion and aggregation at the site of coronary stenting can have catastrophic clinical and economic consequences. Therefore, effective platelet inhibition is vital during and after percutaneous coronary intervention. Eptifibatide is an intravenous antiplatelet agent that blocks the final common pathway of platelet aggregation and thrombus formation by binding to glycoprotein IIb/IIIa receptors on the surface of platelets. In clinical studies, eptifibatide was associated with a significant reduction of mortality, myocardial infarction, or target vessel revascularization in patients with acute coronary syndrome undergoing percutaneous coronary intervention. However, recent trials conducted in the era of dual antiplatelet therapy and
CHAPTER 131 ANTIPLATELET THERAPY Williams Hematology CHAPTER 131 ANTIPLATELET THERAPY HARVEY J. WEISS Antiplatelet Drugs Aspirin Inhibitors of Thromboxane A2 Synthesis or Binding Prostaglandin I2 and Analogues Dipyridamole Ticlopidine and Clopidogrel Inhibitors of the Platelet GPIIB/IIIA Receptor Other Antiplatelet Agents Antiplatelet Drugs in Clinical Medicine Ischemic Heart Disease Valvular Heart Disease Cerebrovascular Disease Peripheral Vascular…
Interactions for ASPIRIN AND EXTENDED-RELEASE DIPYRIDAMOLE (capsule) explain how Aspirin and Extended-Release Dipyridamole works in concert with other medications and substances. This section outlines the advice given to doctors and pharmacists when prescribing and dispensing Aspirin and Extended-Release Dipyridamole
Background: Antiplatelet treatment remains the first choice for primary and secondary prevention of vascular diseases; even so, expected benefits may be offset by risk of bleeding, particularly cerebral hemorrhage. The aim of this study was to assess the influence of antiplatelet treatment on clinical outcome at hospital discharge. Materials and Methods: Consecutive patients with first-ever stroke due to a primary intraparenchymal hemorrhage were prospectively identified over a 4-year period (2000â€2003). Data on hemorrhage location, vascular risk factors, and antiplatelet and anticoagulant treatment were collected. At discharge, outcome was measured using the modified Rankin Scale (disabling stroke ≥3). Patients treated with anticoagulant therapy were excluded from the study. Results: Of 457 consecutive patients with cerebral hemorrhage, 94 (20.5%) had been taking antiplatelet agents. The treated patients (mean age for antiplatelet group 78.9 ± 9.0 years) were older than the ...
The article discusses the therapy for patients with acute coronary syndromes (ACS). It provides information on prasugrel, a new antiplatelet agent which offers an alternative pharmacological treatment and was recently cleared for marketing by the U.S. Food and Drug Administration. It also notes that by inhibiting platelet activation, the thienopyridine antiplatelet agents play a crucial role in the adjunctive treatment of patients with ACS ...
Interactions between heparins, glycoprotein IIb/IIIa antagonists, and coronary intervention. The Global Registry of Acute Coronary Events (GRACE).
... is a platelet aggregation inhibitor. It acts as a reversible cyclooxygenase inhibitor. The Merck Index (12th ed.). p ...
... is a platelet aggregation inhibitor. It works as a thromboxane synthase inhibitor and a thromboxane receptor ... inhibitor, the latter by modifying cellular responses to activation of the thromboxane receptor. Picotamide is licensed in ...
Potent Inhibitors of the Aggregation of Human Platelets". Planta Medica. 51 (4): 300-3. doi:10.1055/s-2007-969496. PMID ...
... is an antispasmodic, vasodilator, and platelet aggregation inhibitor. J. Elks, ed. (2014). The Dictionary of Drugs: ...
... is a platelet aggregation inhibitor. Orefice G, Grasso A, Fazio N, Del Vecchio G, Volpe G, Coppola M, D'Alessio A, ...
... a new inhibitor of thrombroxane A2 induced platelet aggregation". Journal of Biosciences (56): 106-110.. ... elegans induces the aggregation of human platelet cells. M. elegans may also be consumed by amoebae. Bisette, John (1979). " ...
... platelet aggregation inhibitors, which prevent the formation of blood clots; and other anticoagulants. These compounds in their ...
"Design and Synthesis of Piperidine-3-carboxamides as Human Platelet Aggregation Inhibitors". Journal of Medicinal Chemistry. 38 ...
Cinnamtannin B-1 as an antioxidant and platelet aggregation inhibitor. Life sciences, 82(19), 977-982. doi:10.1016/j.lfs. ... and anti-platelet aggregation that may protect damaged tissues in wounds Anderson; Broadhurst, CL; Polansky, MM; Schmidt, WF; ...
"Hawkey C. Inhibitor of platelet aggregation present in saliva of the vampire bat Desmodus rotundus. Br J Haematol.1967;13(6): ...
In molecular biology, ornatin is a potent glycoprotein IIb-IIIa (GP IIb-IIIa) antagonist and platelet aggregation inhibitor ... potent glycoprotein IIb-IIIa antagonists and platelet aggregation inhibitors from the leech Placobdella ornata". Eur. J. ...
... the most potent inhibitor of platelet aggregation. More importantly, PGI2 (and not nitrous oxide) is also associated with an ... "Modulation of human platelet aggregation by the phosphodiesterase type 5 inhibitor sildenafil". Journal of Cardiovascular ... though it prolongs bleeding time by inhibiting collagen-induced platelet aggregation. Another drug, Milrinone, a Type 3 PDE-i ... Phosphodiesterase inhibitors (PDE-i) have been employed with excellent results. It has been shown to reduce mean PAP by as much ...
It acts as a platelet aggregation inhibitor by antagonising the P2Y12 receptor. The drug is produced by AstraZeneca. It was ... Inhibitors of the liver enzyme CYP3A4, such as ketoconazole and possibly grapefruit juice, increase blood plasma levels of ... The Targeting Platelet-Leukocyte Aggregates in Pneumonia With Ticagrelor (XANTHIPPE) study showed improvement in lung function ... Ticagrelor is a weak CYP3A4 inhibitor and is known to increase the concentrations of CYP3A4 metabolised medications; however, ...
... a new platelet aggregation inhibitor produced by Penicillium herquei Fg-372". The Journal of Antibiotics. 49 (1): 50-3. doi: ... a New Platelet Aggregation Inhibitor Produced by Penicillium herquei Fg-372". ChemInform. 27 (27): no. doi:10.1002/chin. ...
... is an analgesic, antipyretic, and anti-inflammatory drug, as well as a platelet aggregation inhibitor. It ...
PGD2 is also involved in smooth muscle contraction/relaxation and is a potent inhibitor of platelet aggregation. This gene is ...
This diverse range of compounds may include: inhibitors of platelet aggregation, ADP, arachidonic acid, thrombin, and PAF. ... Additionally, Ixolaris, a tissue factor inhibitor has been shown to block primary tumor growth and angiogenesis in a ... Ixolaris, a tissue factor inhibitor, blocks primary tumor growth and angiogenesis in a glioblastoma model. J. Thromb. Haemost. ... Tick saliva is a potent inhibitor of endothelial cell proliferation and angiogenesis. Thromb. Haemost. 94, 167e174. Maritz- ...
... is a phosphodiesterase 3 inhibitor which works by inhibiting platelet aggregation and dilating arteries. Cilostazol ... The proton pump inhibitor omeprazole, an inhibitor of CYP2C19, increases exposure to the active metabolite of cilostazol. A ... which is directly related with an inhibition in platelet aggregation. PKA also prevents the activation of an enzyme (myosin ... Serious side effects may include decreased survival in those with heart failure, low platelets, and low white blood cells. ...
Kistrin is a protein inhibitor of platelet aggregation. It belongs to the homologous family of glycoprotein IIb-IIa antagonists ... but platelet aggregation must grow exponentially to form a platelet thrombus and prevent blood loss. Platelet aggregation ... Some thromboregulators enhance platelet aggregation and some others inhibit the process. Platelet aggregation plays a critical ... These inhibitors are substances that prevent the clot formation by preventing platelet adhesion. Platelet inhibition is ...
... common origins for blood coagulation and platelet aggregation inhibitors from soft ticks of the genus Ornithodoros". Molecular ... it inserts its hypostome and prevents the blood from clotting by excreting an anticoagulant or platelet aggregation inhibitor. ...
... is a platelet aggregation inhibitor that was discovered and developed in the Uriach Laboratories, and commercialised ... Triflusal is a selective platelet antiaggregant through; blocks cyclooxygenase, thereby inhibiting thromboxane A2, and thus ... preventing aggregation preserves vascular prostacyclin, thus promoting anti-aggregant effect blocks phosphodiesterase thereby ...
... inhibitors are used clinically as effective inhibitors of adenosine diphosphate-mediated platelet activation and aggregation. ... Angiolillo DJ, Capranzano P (August 2008). "Pharmacology of emerging novel platelet inhibitors". American Heart Journal. 156 (2 ... reversible inhibitor of P2Y12 receptors that causes almost complete inhibition of ADP-induced platelet aggregate. It is a ... impaired platelet turnover, and lung sequestration or apoptosis of overloaded destructive platelets. The dyspnea risks ...
... which is a platelet aggregation inhibitor. It was being developed for secondary prevention of arterial thrombosis following ...
It is also a platelet aggregation inhibitor which is marketed in Spain and Portugal under the trade name Ageroplas. https:// ...
... a potent vasodilator and inhibitor of platelet aggregation. An imbalance of prostacyclin and its physiological antagonist ...
... a potent inhibitor of platelet aggregation from Echis carinatus: synthesis and biological activity of selected analogs". Proc. ...
Aggregation of platelets is highly regulated by cyclic nucleotides. PDE3A is a regulator of this process, and PDE3 inhibitors ... vascular smooth muscle and platelet aggregation. PDE3 inhibitors have been developed as pharmaceuticals, but their use is ... Cilostazol is approved for treatment of intermittent claudication and is thought to involve inhibition of platelet aggregation ... Electronic charges conserve the net charge overall and across the transition state PDE3 inhibitors: antagonize platelet ...
... is a cyclooxygenase inhibitor that was under development for its anti-platelet-aggregation effects. Light P ( ... "Pamicogrel inhibits platelet aggregation". Inpharma Weekly. 1272 (1): 11. January 2001. doi:10.2165/00128413-200112720-00021. ...
t-PA and urokinase are themselves inhibited by plasminogen activator inhibitor-1 and plasminogen activator inhibitor-2 (PAI-1 ... Platelet adhesiveness. Other. *Erythrocyte aggregation. Retrieved from "https://en.wikipedia.org/w/index.php?title=Fibrinolysis ... Factor Xa inhibitors. (with some II inhibition). Heparin group/. glycosaminoglycans/. (bind antithrombin). *Low molecular ... Coagulation inhibitors. *Antithrombin (inhibits II, IX, X, XI, XII). *Protein C (inhibits V, VIII)/Protein S (cofactor for ...
aggregation *Glanzmann's thrombasthenia. *platelet storage pool deficiency *Hermansky-Pudlak syndrome. *Gray platelet syndrome ... Distinguishing a lupus antibody from a specific coagulation factor inhibitor (e.g.: factor VIII) is normally achieved by ... 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 ...
The addition of DAGK inhibitors eliminates the production of [32P]-labeled PA but not the PLD-stimulated production of ... "Phospholipase D activity facilitates Ca2+-induced aggregation and fusion of complex liposomes". Am. J. Physiol. 272 (4 Pt 1): ...
The P-selectin then promotes platelet aggregation through platelet-fibrin and platelet-platelet binding. ... plasma P-selectin concentration was reported to be highly correlated to plasminogen activator inhibitor-1 activity and tissue ... 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 ...
Also there is not as much inhibition of aggregation of platelets. In this case, the greater aggregation of platelets produce ... Organic nitrates should not be taken with PDE5 inhibitors (i.e. sildenafil) since both NO and PDE5 inhibitors increase cyclic ... 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 ... the main inhibitors for most people are phytates (e.g. legumes and cereal grains), but other inhibitors include tannins (from ... Normalization of Hyperhomocysteinemia with Vitamin B12 and Reduction of Platelet Aggregation with n-3 Fatty Acids". Thrombosis ... Non-heme iron is more sensitive to both inhibitors and enhancers of iron absorption: Vitamin C is an iron absorption enhancer; ...
Ristocetin-induced platelet aggregation. .mw-parser-output .nobold{font-weight:normal}. clotting factors:. *Prothrombin time ... hemoglobin ligands also include competitive inhibitors such as carbon monoxide (CO) and allosteric ligands such as carbon ...
Platelet aggregation inhibitor[2]. clopidogrel, ticagrelor -axine. Dopamine and serotonin-norepinephrine reuptake inhibitor[2] ... Angiotensin converting enzyme inhibitor[2]. captopril, lisinopril -oxacin. Quinolone-derived antibiotics. levofloxacin, ...
F. necrophorum produces hemagglutinin which causes platelet aggregation that can lead to diffuse intravascular coagulation and ... Penicillin and penicillin-derived antibiotics can thus be combined with a beta-lactamase inhibitor such as clavulanic acid or ... Platelet count can be low or high. Liver and kidney function tests are often abnormal. ...
The possible exceptions may be aspirin and naproxen due to their anti-platelet aggregation properties. ... Discovery and development of cyclooxygenase 2 inhibitors. Footnotes[edit]. *^ Knox R (September 30, 2004), Merck Pulls ... Other COX-2 inhibitors[edit]. Any increased risk of renal and arrhythmia pathologies associated with the class of COX-2 ... "European Medicines Agency concludes action on COX-2 inhibitors" (PDF). European Medicines Agency. Archived from the original ( ...
... producing an inhibitory effect on platelet aggregation during the lifetime of the affected platelet (8-9 days). This ... Factor Xa inhibitors. (with some II inhibition). Heparin group/. glycosaminoglycans/. (bind antithrombin). *Low molecular ... 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 ...
Beyond this, HRT improves heart contraction, coronary blood flow, sugar metabolism, and decreases platelet aggregation and ... Kuhl, H.; Schneider, H. P. G. (2013). "Progesterone - promoter or inhibitor of breast cancer". Climacteric. 16 Suppl 1: 54-68. ...
... which happens after the initial platelet aggregation and ultimately leads to formation of fibrin and stable aggregated platelet ... Coagulation inhibitor measurementEdit. A Bethesda unit (BU) is a measure of blood coagulation inhibitor activity. It is the ... Direct factor Xa inhibitorsEdit. Main article: Direct Xa inhibitor. Drugs such as rivaroxaban, apixaban and edoxaban work by ... Direct thrombin inhibitorsEdit. Main article: Direct thrombin inhibitor. Another type of anticoagulant is the direct thrombin ...
... thus stimulating platelet and monocyte aggregation around the xenotransplanted organ, causing severe clotting.[32] Additionally ... or C1 inhibitor (C1-INH). Disadvantages of this approach include the toxicity of cobra venom factor, and most importantly these ... 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 ...
Endothelial injury: Injury to the endothelial causing platelet activation and aggregation *Common causes include: trauma, ... Heparin works by binding to and activating the enzyme inhibitor antithrombin III, an enzyme that acts by inactivating thrombin ... A few platelets attach themselves to the valve lips, constricting the opening and causing more platelets and red blood cells to ... The platelet activation causes a cascade of further platelet activation, eventually causing the formation of the thrombus.[4] ...
platelet aggregation. • cell migration. • negative regulation of macrophage derived foam cell differentiation. • activation of ... Coagulation inhibitors. *Antithrombin (inhibits II, IX, X, XI, XII). *Protein C (inhibits V, VIII)/Protein S (cofactor for ... Bennett JS (2001). "Platelet-fibrinogen interactions". Ann. N. Y. Acad. Sci. 936 (1): 340-54. Bibcode:2001NYASA.936..340B. doi: ... platelet-derived growth factor receptor binding. • GO:0001948 protein binding. • identical protein binding. • enzyme binding. • ...
... platelet aggregation, thromboxane formation, and prostacyclin production". Prostaglandins, leukotrienes, and essential fatty ... Increasing DGLA intake may allow DGLA to act as a competitive inhibitor of 2-series PGs and 4-series LTs and thus suppress ...
Caution: bleeding tendencies of unknown origin (indometacin inhibits platelet aggregation). *Caution: Parkinson's disease, ... This is particularly important if Indometacin is given together with an ACE inhibitor or with potassium-sparing diuretics, ... Indometacin, therefore, like other non-selective COX inhibitors can cause peptic ulcers. These ulcers can result in serious ... Indometacin is a nonselective inhibitor of cyclooxygenase (COX) 1 and 2, the enzymes that participate in prostaglandin ...
Endothelial injury: Injury to the endothelium (interior surface of blood vessel), causing platelet activation and aggregation; ... Heparin works by binding to and activating the enzyme inhibitor antithrombin III, an enzyme that acts by inactivating thrombin ... A few platelets attach themselves to the valve lips, constricting the opening and causing more platelets and red blood cells to ... The platelet activation can potentially cause a cascade, eventually leading to the formation of the thrombus.[5] This process ...
platelets: aggregation. *Activation of the 5-HT2A receptor with 2,5-Dimethoxy-4-iodoamphetamine (DOI) produces potent anti- ... 5-HT2A receptor is an adaptive process provoked by chronic administration of selective serotonin reuptake inhibitors (SSRIs) ... In the periphery, it is highly expressed in platelets and many cell types of the cardiovascular system, in fibroblasts, and in ... Cook EH, Fletcher KE, Wainwright M, Marks N, Yan SY, Leventhal BL (August 1994). "Primary structure of the human platelet ...
platelet aggregation. • meiotic spindle organization. • phagocytosis, engulfment. • negative regulation of actin filament ... ACE-inhibitors or angiotensin II receptor blockers may be effective in reducing proteinuria when given at the early stage of ... Platelets of MYH9-RD patients are characterized by a very large size: platelets larger than red blood cells (called "giant ... platelet formation. • leukocyte migration. • establishment of meiotic spindle localization. • blood vessel endothelial cell ...
... produced by platelet cells) are vasoconstrictors and facilitate platelet aggregation. Their name comes from their role in clot ... COX-2 selective inhibitors or coxibs. *Cyclopentenone prostaglandins may play a role in inhibiting inflammation ... Prostaglandins are powerful locally acting vasodilators and inhibit the aggregation of blood platelets. Through their role in ... "Activation of the murine EP3 receptor for PGE2 inhibits cAMP production and promotes platelet aggregation". The Journal of ...
Aggregation of thrombocytes (platelets). Platelet-rich human blood plasma (left vial) is a turbid liquid. Upon addition of ADP ... When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead ... Platelet plug formation- Platelets adhere to damaged endothelium to form a platelet plug (primary hemostasis) and then ... When platelets are activated, they express glycoprotein receptors that interact with other platelets, producing aggregation and ...
Mosquito saliva negatively affects vascular constriction, blood clotting, platelet aggregation, angiogenesis and immunity, and ... such as clotting inhibitors and capillary dilators, that could be useful for cardiovascular disease. ... creates inflammation.[៦៣] Universally, hematophagous arthropod saliva contains at least one anti-clotting, one anti-platelet, ...
Arterial thrombosis is platelet-rich, and inhibition of platelet aggregation with antiplatelet drugs such as aspirin may reduce ... Other medications such as direct thrombin inhibitors and direct Xa inhibitors are increasingly being used instead of warfarin.[ ... Instead, the platelet-derived growth factor degranulated by the clotted platelets will attract a layer of smooth muscle cells ... When a blood vessel (a vein or an artery) is injured, the body uses platelets (thrombocytes) and fibrin to form a blood clot to ...
... bleeding due to inhibition of platelet aggregation, and tachycardia.[16][17] Clinical use of these agonists is contraindicated ... These agonists might produce more effective inhibitor results on airways allergic diseases but their toxicity (e.g. pulmonary ... the loss of IP's anti-platelet activity.[12][13] IP activation of animal and human platelets inhibits their aggreatation ... PlateletsEdit. IP gene knockout mice (i.e. IP(-/-) mice) exhibit increased tendency to thrombosis in response to experimentally ...
Prostacyclin usually prevents platelet aggregation and vasoconstriction, so its inhibition can lead to excess clot formation ... of NSAID expenditures were for COX-2 inhibitors. Over the period of the study, COX-2 inhibitors rose from 10.03% of total ... "COX-2 Inhibitors and Cancer". Fact Sheet. United States National Cancer Institute. Archived from the original on May 9, 2008.. ... COX-2 inhibitors appear to work as well as nonselective NSAIDS.[5] They have not been compared to other treatment options such ...
"U.S. FDA Approved Immune-Checkpoint Inhibitors and Immunotherapies". Medical Writer Agency , 香港醫學作家 , MediPR , MediPaper Hong ... Scanning electron micrograph of a red blood cell (left), a platelet (center), and a T lymphocyte (right) ... which allows the aggregation of signalling complexes around these proteins. ...

No data available that match "platelet aggregation inhibitors"


  • It has been observed, by comparing the efficacy of heparin to those of direct thrombin inhibitors (direct inhibitor means an inhibitor which inhibits thrombin without requiring AT III), that they are much more effective than heparin for preventing and treating arterial thrombosis (Arteriosclerosis and thrombosis, 1992, 12, 879-885, J. Am. Coll. (allindianpatents.com)
  • The reason for this lack of efficacy is that the heparin/AT III complex cannot, for reasons to do with steric hindrance, inhibit thrombin in a thrombus rich in platelets as is a platelet thrombus. (allindianpatents.com)
  • The low activity of heparin in contrast to direct inhibitors is therefore linked to its need to use AT III. (allindianpatents.com)
  • If anti-PF4/heparin antibodies (anti-PF4/Hep Abs) are present, 2 strategies exist to prevent intraoperative aggregation during bypass surgery: first, using an alternative anticoagulant, and second, using heparin combined with an antiaggregant. (anesthesiaexperts.com)
  • The present in vitro study evaluated cangrelor's ability to inhibit heparin-induced platelet aggregation in the presence of anti-PF4/Hep Abs. (anesthesiaexperts.com)
  • Light transmission aggregometry was used to measure platelet aggregation after adding 0.5 IU·mL −1 of heparin (HIT) to the plasma, and this was compared with samples spiked with normal saline (control) and samples spiked with cangrelor 500 ng·mL −1 and heparin 0.5 IU·mL −1 (treatment). (anesthesiaexperts.com)
  • Heparin 0.5 IU·mL −1 triggered aggregation in 22 of 44 PPP-PRP mixtures, with a median aggregation of 86% (interquartile range [IQR], 69-91). (anesthesiaexperts.com)
  • 001). Cangrelor inhibited heparin-induced aggregation by a median of 91% (IQR, 52-100). (anesthesiaexperts.com)
  • This in vitro study found that cangrelor was an unreliable inhibitor of heparin-induced aggregation in the presence of anti-PF4/Hep Abs. (anesthesiaexperts.com)
  • Potent inhibitors of platelet aggregation based upon the Arg-Gly-Asp-Phe sequence of fibrinogen. (nih.gov)
  • Platelet activation by thrombin was only slightly suppressed by polymyxin B, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) or staurosporine, all being potent inhibitors of PKC in vitro. (uni-regensburg.de)
  • The study suggests that ginsenosides Rk1 and Rg5 can be potent platelet aggregation inhibitors. (redsenolhealth.com)
  • Potent inhibitors of the aggregation of human platelets. (nature.com)
  • Two congeners of N-{[3-(1,1'-biphenyl-4-yl)methoxy]phenyl}piperidine-4-carboxamide (7m and 7p) proved to be potent FXa-selective inhibitors (K(i) = 130 and 57 nM, respectively) and antiplatelet agents and were identified as leads for developing new dual function antithrombotic drugs. (uniba.it)
  • This interaction activates intracellular signals that promote the release of adenosine diphosphate (ADP), adrenaline, serotonin, thrombin and thromboxane A2, potent agonists of platelet activation. (scielo.br)
  • Nicardipine and dipyridamole were the most potent BCRP inhibitors among the compounds tested with IC50 values of 4.8 +/- 1.3 and 6.4 +/- 0.9 microM, respectively. (biomedsearch.com)
  • 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. (innovations-report.com)
  • Thrombin, 1-oleoyl-2-acetyl-rac-glycerol (OAG), cis- or trans-octadecadienoic acids (linoleic and linolelaidic acid) and the synergistic combination of octadecadienoic acids plus OAG lead to the activation of gel-filtered human platelets, i.e. aggregation via protein kinase C (PKC). (uni-regensburg.de)
  • Phosphorylase activity in suspensions of human platelets has been assayed before and after addition of thrombin and epinephrine which aggregate platelets, prostaglandins E 1 and E 2 and dibutyryl-3′,5′-AMP which inhibit aggregation, or sodium fluoride and isoproterenol which alter adenine nucleotide metabolism. (elsevier.com)
  • Pretreatment with indomethacin in vitro attenuated spontaneous platelet aggregation without affecting CF6-induced increase in small-sized aggregates. (ahajournals.org)
  • Our results indicate (1) that the ability of various compounds to inhibit PKC in vitro does not correlate with their inhibitory effects in intact cells and (2) that platelet activation induced by various PKC activators exhibits differential PKC-inhibitor sensitivity. (uni-regensburg.de)
  • In order to determine which drugs would be most effective as inhibitors of platelet release and aggregation, In vitro release reactions and platelet aggregometry were used to evaluate aspirin, dipyridamole, sulfinpyrazone, flurbiprofen, low molecular weight dextran (dextran 40), prostaglandin E, (PGE 1 ), apyrase, and adenosine. (jamanetwork.com)
  • In vitro studies suggest that sulfinpyrazone is one of the most effective of platelet inhibitors currently available for clinical testing. (jamanetwork.com)
  • Platelets probably become "exhausted" following chronic endogenous activation, with decreased response when aggregation is analyzed in vitro. (pvrinstitute.org)
  • A series of benzyloxy anilides of nipecotic (5, 6) and isonipecotic (7, 8) acids were synthesized and assayed in vitro as inhibitors of ADP-induced platelet aggregation and the blood coagulation enzymes factor Xa (FXa) and thrombin (FIIa). (uniba.it)
  • In vitro and in vivo platelet assays (aggregation, flow and other functional tests) were also employed, using both human and murine platelets. (greenmedinfo.com)
  • SFN inhibited collagen-mediated platelet aggregation in vitro and in vivo and the associated adhesion and impaired calcium signalling. (greenmedinfo.com)
  • Thrombomodulin alfa prevents the decrease in platelet aggregation in rat models of disseminated intravascular coagulation. (bioportfolio.com)
  • Disseminated intravascular coagulation (DIC), a deadly complication characterized by uncontrolled hypercoagulation, causes a decrease in the platelet count and impairs platelet aggregation. (bioportfolio.com)
  • The patent awarded covers the basic composition of TP-9201, a platelet aggregation inhibitor , and related compositions for the treatment of thrombosis," said Dr. (thefreedictionary.com)
  • 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. (umassmed.edu)
  • Thrombin inhibitors therefore constitute an effective means of preventing or combating this type of thrombosis. (allindianpatents.com)
  • This explanation is further justified by the recent observation that the direct inhibitors of factor Xa which act without AT III are also effective, in animal models of arterial thrombosis (Circulation, 1991, 84, 1741-1748 Thrombosis Haemost. (allindianpatents.com)
  • Methods for their use, such as to prevent thrombosis without increasing hemorrhage, enhancing the survivability of platelets during storage or transfusion and to attenuate ischemia-reperfusion injury (IPI), are also provided. (google.com)
  • Platelet activation plays a major role in hemostasis and thrombosis. (bioportfolio.com)
  • Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. (bioportfolio.com)
  • Objective ADAMTS13 inhibits platelet aggregation and arterial thrombosis by cleavage of von Willebrand factor (VWF). (bio-aromatica.com)
  • Platelet activation provides a critical link between inflammation and thrombosis. (greenmedinfo.com)
  • As inflammation promotes thrombosis and vice versa, in this study we investigated whether SFN is able to reduce inflammatory potentiation of thrombotic events, suppress platelet activation and thrombus formation in the cerebral microvasculature. (greenmedinfo.com)
  • Plavix (clopidogrel), a platelet aggregation inhibitor , is BMS' largest selling product and continues to make substantial year-on-year sales growth. (thefreedictionary.com)
  • Dosing of clopidogrel for platelet inhibition in infants and young children: primary results of the Platelet Inhibition in Children On cLOpidogrel (PICOLO) trial. (clinicaltrials.gov)
  • This study is designed to provide data on platelet aggregation of PA32540 plus clopidogrel dosed separately compared to EC aspirin 81 mg plus EC omeprazole 40 mg plus clopidogrel dosed concomitantly. (clinicaltrials.gov)
  • New highly active antiplatelet agents with dual specificity for platelet P2Y1 and P2Y12 adenosine diphosphate receptors. (umassmed.edu)
  • New antiplatelet agents that provide greater, more consistent inhibition of the platelet ADP receptor P2Y12 may be used in combination with glycoprotein (GP) IIb-IIIa antagonists, but their combined effect on platelet function and procoagulant activity is not well studied. (nih.gov)
  • preventive administration of NADPH in the rats can remarkably inhibit Thrombin-induced platelet aggregation. (wipo.int)
  • First of all, the result of algae or sponges upon platelet aggregation was examined and they didn't inhibit collagen-induced platelet aggregation on platelet wealthy plasma (PRP) (data not really shown). (bioriental.net)
  • The ingredients of Dm-H-SP and Dm-Ac-PF didn't inhibit aggregation of WP induced by thrombin (Body 2A) or collagen (Body 2B), despite having 10 min incubation (data not really proven). (bioriental.net)
  • Another two sponges (Computer, Av) didn't inhibit aggregation either at 2 min or 10 min incubation. (bioriental.net)
  • Both parent drug and its active metabolite inhibit platelet aggregation by reversibly interacting with platelet P2Y 12 ADP-receptors, preventing signal transduction and platelet activation. (thefreedictionary.com)
  • 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. (thefreedictionary.com)
  • The complementary effects of abciximab and R-138727 on platelet activation, aggregation, and procoagulant activity suggest their combined use may, to a greater degree than with either agent alone, reduce thrombus formation in vivo. (nih.gov)
  • Glenzocimab (ACT017) is a humanized monoclonal antigen-binding fragment (Fab) directed against the human platelet glycoprotein VI, a key receptor for collagen and fibrin that plays a major role in thrombus growth and stability. (acticor-biotech.com)
  • This means that in patients with high thrombus burden, tirofiban is more suited to provide a full antithrombotic activity than cangrelor, which unlike tirofiban, is not associated with a rebound in platelet reactivity after drug infusion discontinuation. (cardiovascularnews.com)
  • When a blood vessel receives an injury, the platelets binding to fibrinogen will initiate aggregation and form a thrombus. (justia.com)
  • Inhibitors of this interaction are useful in modulating platelet thrombus formation. (justia.com)
  • Once platelets are activated, glycoprotein IIb-IIIa complexes bind to fibrinogen to constitute the final stage of platelet aggregation and thrombus formation. (scielo.br)
  • Platelet Aggregation Inhibitors are herbs that prevent platelets from collecting at a point in the blood vessels to make a clot. (herbpathy.com)
  • Brilinta belongs to a group of drugs called antiplatelet medications, which help prevent platelets from forming clots that could lead to heart attacks and strokes. (rxwiki.com)
  • CF6 enhanced spontaneous micro-aggregation of platelets through ecto-F 1 F o complex in patients with recent onset stroke independently of anti-platelet therapy. (ahajournals.org)
  • CF6 can be a novel target molecule in anti-platelet therapy against cardiovascular events in humans. (ahajournals.org)
  • The subject of the present invention related to a combination of direct or indirect selective inhibitors of factor Xa which act via antithrombin III, in combination with a compound with anti-platelet aggregation activity, for their activity in arterial thromboembolic diseases. (allindianpatents.com)
  • The pharmaceutical compositions containing the combination of antithrombotic and anti-platelet aggregation active ingredients are also included in the invention. (allindianpatents.com)
  • It has now been found, according to the present invention, quite surprisingly, that a direct or indirect selective inhibitor of factor Xa, alone or in combination with a compound with anti-platelet aggregation activity, can be used for their activity in thromboembolic diseases of arterial origin. (allindianpatents.com)
  • It is an anti-platelet agent, designed to decrease the tendency of platelets to clump together to form a blood clot. (rxwiki.com)
  • High-intensity intermittent exercise increases adenosine hydrolysis in platelets and lymphocytes and promotes platelet aggregation in futsal athletes. (bioportfolio.com)
  • A proposal on the nature of the binding interaction between the Asp-carboxylate of RGDX mimetics and the platelet GP IIb-IIIa receptor. (nih.gov)
  • Antagonists of fibrinogen at the GPIIb/IIIa receptor, which is the most abundant membrane protein on the platelet surface, are under active investigation as potential antithrombotics. (openarchives.gr)
  • GM1CD9 triggers platelet activation resulted in platelet aggregation, but it is blocked by anti-Fc receptor CD32. (dansukyoshitsu-park.com)
  • The renin-angiotensin system blockers segment is further classified into ACE inhibitors and angiotensin receptor blockers and the anti-clotting agents segment is further segmented into anti-coagulants and platelet aggregation inhibitors. (express-press-release.net)
  • P-selectin, soluble endothelial protein C receptor, soluble thrombomodulin, plasminogen activator inhibitor 1, ADAMTS-13, von Willebrand factor, tissue factor, soluble intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 were more elevated in LF patients than in controls. (cdc.gov)
  • Endothelial protein C receptor, thrombomodulin, intercellular adhesion molecule 1, plasminogen activator inhibitor 1, D-dimer, and hepatocyte growth factor were higher in fatal than nonfatal LF cases. (cdc.gov)
  • It works as a thromboxane synthase inhibitor and a thromboxane receptor inhibitor, the latter by modifying cellular responses to activation of the thromboxane receptor. (wikipedia.org)
  • Healthy donor blood was treated with the active metabolite of prasugrel (R-138727 5 μmol/L), GPIIb-IIIa antagonists (abciximab 3 μg/mL or eptifibatide 0.9 μg/mL), and combinations thereof, exposed to physiologically relevant agonists (collagen and ADP) and then evaluated for markers of platelet activation and procoagulant activity. (nih.gov)
  • R-138727 and the GPIIb-IIIa antagonists had additive inhibitory effects on collagen-stimulated platelet aggregation and on the collagen plus ADP-stimulated level of activated platelet surface GPIIb-IIIa. (nih.gov)
  • No. 4,683,291, inhibition of platelet function is disclosed with synthetic peptides designed to be high affinity antagonists of fibrinogen binding to platelets. (justia.com)
  • In order to evaluate the involvement of monoaminergic system, rats were pretreated with the inhibitor of brain serotonin stores p-chlorophenylalanin (PCPA), dopamine (SCH23390 and sulpiride), and adrenoceptor (prazosin and propranolol) antagonists. (bireme.br)
  • Two combinations of agonists, 0.5 micromol/l 5-HT plus 3 micromol/l epinephrine, and 1 micromol/l 5-HT plus 3 micromol/l epinephrine, were used to induce platelet aggregation. (nih.gov)
  • After that, adenosine diphosphate (ADP) (15 M) was put into induce platelet aggregation. (bioriental.net)
  • L-arginine infusion decreases peripheral arterial resistance and inhibits platelet aggregation in healthy subjects. (greenmedinfo.com)
  • Sarpogrelate is an antiplatelet agent that decreases 5-hydroxytryptamine( 5-HT )levels in platelets via blockade of 5-HT2 receptors, has been used in atherosclerotic peripheral arterial disease. (clinicaltrials.gov)
  • 2. The method of claim 1 , wherein the PS-binding agent inhibits the attachment of monocytes or platelets that express receptors for PS to ischemic or activated cells, and wherein the ischemic or activated cells express PS on their cell surface. (google.com)
  • Actually, a more proclaimed inhibitory influence on aggregation induced by thrombin or collagen could possibly be noticed for the remove of alga Dc-H (Body 2A,B). Distinctions in the inhibitory profile could be described by the actual fact that thrombin and collagen usually do not buy Mogroside IVe talk about exactly the same receptors [36]. (bioriental.net)
  • Epoprostenol has two major pharmacological actions: (1) direct vasodilation of pulmonary and systemic arterial vascular beds, and (2) inhibition of platelet aggregation. (pharmacycode.com)
  • Only 28% of all patients in the trial, sponsored by Ortho Biotech Clinical Affairs, were on a platelet aggregation inhibitor such as aspirin. (thefreedictionary.com)
  • Policosanol (20 mg day) is as effective as aspirin (100 mg day) as a platelet aggregation inhibitor. (greenmedinfo.com)
  • Collagen and epinephrine-induced release and aggregation were inhibited by the same drugs as well as by aspirin and apyrase. (jamanetwork.com)
  • Platelet aggregation time was significantly (P less than 0.01) decreased in female rabbits treated with oral contraceptive (a preparation containing low dose of estrogen) as also by injection of diethylstilbestrol (10 mg/kg), while in animals that received indomethacin (10 mg/kg) or aspirin (30 mg/kg) (PG synthetase inhibitors) along with oral contraceptives or diethylstilbestrol there was no significant alteration in platelet aggregation time. (who.int)
  • 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. (bioportfolio.com)
  • 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. (bioportfolio.com)
  • Antiplatelet drugs, such as aspirin, prevent blood cells called platelets from clumping together to form a clot. (medlineplus.gov)
  • Glycoprotein IIb/IIIa inhibitor (tirofiban) in acute ST-segment elevation myocardial infarction. (biomedsearch.com)
  • Studies have shown conflicting results for glycoprotein IIb/IIIa inhibitor (tirofiban) use in ST-segment elevation myocardial infarction (STEMI). (biomedsearch.com)
  • The critical interaction between GPIIb/IIIa and fibrinogen can be inhibited by either linear or cyclic RGDS-containing peptides, which have been proved as lead compounds in the design of platelet aggregation inhibitors. (openarchives.gr)
  • Fibrinogen binding to platelets is important to normal platelet function in the blood coagulation mechanism. (justia.com)
  • Other synthetic peptides and their use as inhibitors of fibrinogen binding to platelets are disclosed by Koczewiak et al. (justia.com)
  • Coller, 1980 "Interaction of normal, thrombasthenic, and Bernard-Soulier platelets with immobilized fibrinogen: defective platelet-fibrinogen interaction in thrombasthenia," Blood 55:169-178. (freepatentsonline.com)
  • 1987, "Arginyl-glycyl-aspartic acid sequences and fibrinogen binding to platelets", Blood 70:110-115. (freepatentsonline.com)
  • Inhibits fibrinogen interaction with platelets. (uniprot.org)
  • Sarpogrelate treatment inhibited platelet aggregation dose-dependently in patients with ischemic stroke, as judged by a new assessment system employing combinations of 5-HT and epinephrine as agonists. (nih.gov)
  • The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage. (google.com)
  • Future studies in patients with ischemic stroke are now needed to establish the relationship between ex vivo platelet aggregation and the clinical effect. (acticor-biotech.com)
  • The ischemic disorders, where platelet aggregation and bloodstream coagulation are participating, represent a significant reason behind disability and death worldwide. (bioriental.net)
  • To test the hypothesis that the modification of platelet behavior might reduce the incidence of ischemic deficits following surgery for subarachnoid hemorrhage. (strokecenter.org)
  • Saratin, an inhibitor of von Willebrand factor-dependent platelet adhesion, decreases platelet aggregation and intimal hyperplasia in a rat carotid endarterectomy model. (hirudoshop.com)
  • Proton pump inhibitor, decreases accumulation of acid in gastirc lumen / c decrease GERD, healing of duodenal ulcers. (flashcardmachine.com)
  • Light intensities of small (9-25μ n), medium (25-50μ m), and large (50-70μ m) platelet aggregates were measured by the laser light scattering aggregometer (PA-200C) with or without adenosine diphosphate (ADP, 2μ M) or collagen (1μ g/ml). (ahajournals.org)
  • Adenosine diphosphate-induced aggregation was most effectively inhibited by PGF 1 , sulfinpyrazone, and dipyridamole. (jamanetwork.com)
  • The isothiocyanate sulforaphane modulates platelet function and protects against cerebral thrombotic dysfunction. (greenmedinfo.com)
  • 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. (ebi.ac.uk)
  • 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. (umassmed.edu)
  • The OAG-induced aggregation, however, was strongly inhibited by H-7 or staurosporine but not by polymyxin B. In contrast, octadecadienoic acid-induced aggregation was substantially inhibited only by polymyxin B. Synergistic activation by OAG plus octadecadienoic acids was strongly suppressed by all three PKC inhibitors. (uni-regensburg.de)
  • We speculate that this might be due to improvement of chronic endogenous platelet activation. (pvrinstitute.org)
  • Reduced β2-GPI is associated with increased platelet aggregation and activation in patients with prolonged isolated thrombocytopenia after allo-HSCT. (bioportfolio.com)
  • Platelet activation is an essential event that is. (bioportfolio.com)
  • Characterization of distinct mechanism of agonist-induced canine platelet activation. (bioportfolio.com)
  • migration and platelet activation. (dansukyoshitsu-park.com)
  • CD9 antigen modulates cell adhesion, migration and platelet activation. (dansukyoshitsu-park.com)
  • Situations involving injury and discontinuation of the endothelial lining stimulate the adhesion, activation, and aggregation of platelets, culminating in the formation of arterial or venous thrombi. (scielo.br)
  • RGD peptide products under development include a cell adhesive coating designed to improve the performance of implantable devices and their acceptance by the body, and a platelet aggregation inhibitor designed to prevent unwanted blood clotting without causing bleeding at therapeutic doses, unlike certain therapies now existing or under development by others. (thefreedictionary.com)
  • Platelet aggregation inhibitors are also known as antiplatelet drugs. (edrugsearch.com)
  • These drugs prevent the platelets in your blood from gathering together in big groups, which can cause blood clots. (edrugsearch.com)
  • Based on drug class the global cardiovascular drugs market is segmented into renin-angiotensin system blockers, beta blockers, diuretics, anti-clotting agents (anti-coagulants and platelet aggregation inhibitors), antihyperlipidemics, other antihypertensive, calcium channel blockers and others. (express-press-release.net)
  • The present invention is based on the surprising discovery that erythrocytes conjugated to certain peptides and polypeptides containing an R-G-D (Arg-Gly-Asp) sequence (collectively termed herein "RGD peptides") according to the invention, selectively bind to activated platelets but not to unactivated platelets. (freepatentsonline.com)
  • This protein strongly inhibited ADP-induced platelet aggregation in rabbit platelet-rich plasma (PRP), and its IC50 was about 58 nM. (ovid.com)
  • This protein promptly dissociated platelet aggregation in rabbit PRP stimulated by high-concentration ADP. (ovid.com)
  • PURPOSE: We investigated whether dipyridamole and various calcium channel blockers are inhibitors and/or substrates of breast cancer resistance protein (BCRP). (biomedsearch.com)
  • Gene Ontology (GO) annotations related to this gene include identical protein binding and platelet-derived growth factor binding . (genecards.org)
  • The impaired homeostasis and platelet dysfunction implicate alterations in the protein C pathway, which might contribute to the loss of endothelial barrier function in fatal infections. (cdc.gov)
  • 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). (bioportfolio.com)
  • In the long term, Eli Lilly owns a robust late-stage drug pipeline including Arxxant for diabetic retinopathy and Prasugrel, a platelet aggregation inhibitor in the same mechanistic class as Plavix (Bristol-Myers Squibb;BMY/Sanofi-Aventis;SNY) for cardiovascular disease. (thefreedictionary.com)
  • This latter finding likely reflects the fast recovery of platelet function at the end of cangrelor infusion and the time needed for prasugrel to provide sufficient IPA once cangrelor infusion is terminated," they add. (cardiovascularnews.com)
  • The second take-home message is that chewing standard loading dose of prasugrel is associated with a marginal and not significant increase in platelet inhibition, which is unlikely to translate into a clinically meaningful difference. (cardiovascularnews.com)
  • It inhibited ristocetin-induced platelet aggregation in rabbit PRP (IC50: 100 nM), but hardly blocked collagen-induced platelet aggregation. (ovid.com)
  • R-138727 and abciximab each inhibited collagen plus ADP-stimulated platelet phosphatidylserine expression and prothrombin cleavage, and the combination produced greater inhibition than achieved with abciximab alone. (nih.gov)
  • The PK/PD model thus described glenzocimab plasma concentrations and its effects on ex vivo collagen-induced platelet aggregation. (acticor-biotech.com)
  • which fact may describe why algae or sponges inhibited just the ADP-induced aggregation, however, not the collagen one. (bioriental.net)
  • Dc-AC inhibited 20% and 35% aggregation induced by thrombin (Body 2A) or collagen (Body 2B), respectively. (bioriental.net)
  • However when the algae Dc-H, Dm-H-PF, Dc-AC and Dm-DC had been incubated with WP for 10 min, the inhibitory aftereffect of them on platelet aggregation induced by collagen or thrombin was doubled (data not really proven). (bioriental.net)
  • Four of ten sponges (De, Av, Hh and Af) inhibited aggregation of WP induced by thrombin (Body 2C) or collagen (Body 2D) after 2 min of incubation. (bioriental.net)
  • Acts by binding to alpha-IIb/beta-3 (ITGA2B/ITGB3) on the platelet surface and inhibits aggregation induced by ADP, thrombin, platelet-activating factor and collagen. (uniprot.org)
  • The remove of Pc didn't hinder platelet aggregation induced by both agonists (Statistics 2C,D). Open up in another window Open up in another window Body 2. (bioriental.net)
  • B01AC Platelet aggregation inhibitors excl. (genome.jp)
  • Platelet Aggregation Inhibitors" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • Ginsenosides Rk1 and Rg5 exert inhibitory effects on arachidonic acid (AA)-induced platelet aggregation in a dose-dependent manner, according to a study published in the Journal Pharmazie . (redsenolhealth.com)
  • Reference values of platelet aggregometry in healthy subjects. (bioportfolio.com)
  • Drug that inhibits platelets from aggregating to form a plug. (thefreedictionary.com)
  • The results showed that Ginsenoside Rk1 and Rg5 were found to be 8-22 fold more inhibitory against platelet aggregation than that of a known antiplatelet drug acetylsalicylic acid, but ginsenoside 20(S)-Rg3 and 20(R)-Rg3 showed poor inhibitory activity. (redsenolhealth.com)
  • Anti-aggregation effect on platelets of Indiplon a hypnotic sedative non-benzodiazepine drug. (bioportfolio.com)
  • acute coronary syndrome, prophylaxis (and more ), and belongs to the drug class platelet aggregation inhibitors. (drugs.com)
  • A natural cardioprotective functional ingredient exhibits antiinflammatory, angiotensin-converting enzyme inhibitory, and anti-aggregation properties. (greenmedinfo.com)
  • Spontaneous platelet micro-aggregation is a marker for the prognosis of patients with cardiovascular diseases. (ahajournals.org)
  • The present double-blind controlled clinical pharmacology study was performed on 45 patients with cerebral infarction, who were given 75, 150, or 300 mg three times daily of sarpogrelate for 7 days in order to evaluate the dose-response relationship in terms of the precisely measured inhibition of platelet aggregation. (clinicaltrials.gov)
  • 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. (clinicaltrials.gov)
  • To mitigate upper gastrointestinal bleeding events, these patients would require the use of a proton pump inhibitor. (clinicaltrials.gov)
  • The FABOLUS FASTER trial, which was presented at PCR e-Course 2020 and simultaneously published in Circulation , shows that cangrelor provides inferior inhibitor of platelet aggregation (IPA) to tirofiban in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI). (cardiovascularnews.com)
  • Therefore, the final message from the study is that only parenteral agents are able to provide early inhibition of platelet reactivity among STEMI patients and yet the various antiplatelet parenteral options should not be seen as class agents considering that their potency and efficacy largely differ. (cardiovascularnews.com)
  • Platelet-poor plasma (PPP) from 30 patients with functional anti-PF4/Hep Abs was mixed with platelet-rich plasma (PRP) from 5 healthy donors. (anesthesiaexperts.com)
  • In Sierra Leone during 2015-2018, we assessed LF patients' day-of-admission plasma samples for levels of proteins necessary for coagulation, fibrinolysis, and platelet function. (cdc.gov)
  • Kiwifruit consumption reduces platelet aggregation and blood triglycerides in human subjects. (greenmedinfo.com)
  • If a blood vessel is ruptured, platelets collect at the point of tear and block the leak till the blood vessel is repaired. (herbpathy.com)
  • Platelet are blood cells and platelet aggregation is the biological process which is functioned as bleeding inhibitor. (redsenolhealth.com)
  • It participates in platelet aggregation and fibrin formation in the blood clotting mechanism. (justia.com)
  • Platelets are cellular elements found in whole blood which also participate in blood coagulation. (justia.com)
  • They can be used as bronchodilators and/or inhibitors of blood-platelet aggregation. (google.com)
  • tell your doctor if you have bleeding ulcers (sores in the lining of the stomach or small intestine that are bleeding), bleeding in the brain, bleeding from any other part of your body, a low number of platelets in your blood, or any other condition that causes severe bleeding. (medlineplus.gov)
  • For that reason, the reference arm in this study uses Prilosec® 40 mg as a comparator - the same proton pump inhibitor at the same dose level. (clinicaltrials.gov)
  • Omeprazole is a proton pump inhibitor (PPI). (drugs.com)
  • There was a mild decrease in platelet count (p=0.093), particularly in the sildenafil group. (pvrinstitute.org)
  • Disorder characterized by a decrease or lack of platelet dense bodies in which the releasable pool of adenine nucleotides and 5HT are normally stored. (bioportfolio.com)
  • Curiously, a 10% decrease in the inhibitory impact was observed once the sponges De, Hh or Af had been incubated with platelets for 10 min (data not really shown). (bioriental.net)
  • Thrombocytopenia is a common feature of hemorrhagic fevers and vascular permeability disorders ( 8 ), but the decrease in platelet counts in acute LF is not low enough to cause spontaneous hemorrhage. (cdc.gov)
  • Therefore, the objective of this study was to evaluate the independent and complementary effects of P2Y12 and GPIIb-IIIa inhibition on platelet function and procoagulant activity. (nih.gov)
  • No. 11/486,667, "Modified Annexin Proteins And Methods For Their Use In Platelet Storage And Transfusion," pending, filed Jul. (google.com)
  • Situations involving injury and discontinuation of the endothelial lining stimulate platelet adhesion to subendothelial matrix proteins. (scielo.br)
  • Of particular interest is a class of phenyl amidine derivatives useful as inhibitors of platelet aggregation. (justia.com)