Indomethacin. Medical search

A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.

Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.

A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.

Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.

The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.

(11 alpha,13E,15S)-11,15-Dihydroxy-9-oxoprost-13-en-1-oic acid (PGE(1)); (5Z,11 alpha,13E,15S)-11,15-dihydroxy-9-oxoprosta-5,13-dien-1-oic acid (PGE(2)); and (5Z,11 alpha,13E,15S,17Z)-11,15-dihydroxy-9-oxoprosta-5,13,17-trien-1-oic acid (PGE(3)). Three of the six naturally occurring prostaglandins. They are considered primary in that no one is derived from another in living organisms. Originally isolated from sheep seminal fluid and vesicles, they are found in many organs and tissues and play a major role in mediating various physiological activities.

Enzyme complexes that catalyze the formation of PROSTAGLANDINS from the appropriate unsaturated FATTY ACIDS, molecular OXYGEN, and a reduced acceptor.

Compounds that inhibit the action of prostaglandins.

A congenital heart defect characterized by the persistent opening of fetal DUCTUS ARTERIOSUS that connects the PULMONARY ARTERY to the descending aorta (AORTA, DESCENDING) allowing unoxygenated blood to bypass the lung and flow to the PLACENTA. Normally, the ductus is closed shortly after birth.

A constitutively-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes.

A dual inhibitor of both cyclooxygenase and lipoxygenase pathways. It exerts an anti-inflammatory effect by inhibiting the formation of prostaglandins and leukotrienes. The drug also enhances pulmonary hypoxic vasoconstriction and has a protective effect after myocardial ischemia.

Ulceration of the GASTRIC MUCOSA due to contact with GASTRIC JUICE. It is often associated with HELICOBACTER PYLORI infection or consumption of nonsteroidal anti-inflammatory drugs (NSAIDS).

A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis.

Lining of the STOMACH, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. The surface cells produce MUCUS that protects the stomach from attack by digestive acid and enzymes. When the epithelium invaginates into the LAMINA PROPRIA at various region of the stomach (CARDIA; GASTRIC FUNDUS; and PYLORUS), different tubular gastric glands are formed. These glands consist of cells that secrete mucus, enzymes, HYDROCHLORIC ACID, or hormones.

The physiologically active and stable hydrolysis product of EPOPROSTENOL. Found in nearly all mammalian tissue.

A potent lipoxygenase inhibitor that interferes with arachidonic acid metabolism. The compound also inhibits formyltetrahydrofolate synthetase, carboxylesterase, and cyclooxygenase to a lesser extent. It also serves as an antioxidant in fats and oils.

A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.

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.

(9 alpha,11 alpha,13E,15S)-9,11,15-Trihydroxyprost-13-en-1-oic acid (PGF(1 alpha)); (5Z,9 alpha,11,alpha,13E,15S)-9,11,15-trihydroxyprosta-5,13-dien-1-oic acid (PGF(2 alpha)); (5Z,9 alpha,11 alpha,13E,15S,17Z)-9,11,15-trihydroxyprosta-5,13,17-trien-1-oic acid (PGF(3 alpha)). A family of prostaglandins that includes three of the six naturally occurring prostaglandins. All naturally occurring PGF have an alpha configuration at the 9-carbon position. They stimulate uterine and bronchial smooth muscle and are often used as oxytocics.

The relationship between the dose of an administered drug and the response of the organism to the drug.

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).

An inducibly-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes and INFLAMMATION. It is the target of COX2 INHIBITORS.

Compounds that bind to and inhibit that enzymatic activity of LIPOXYGENASES. Included under this category are inhibitors that are specific for lipoxygenase subtypes and act to reduce the production of LEUKOTRIENES.

A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.

A synthetic prostaglandin E analog that protects the gastric mucosa, prevents ulceration, and promotes the healing of peptic ulcers. The protective effect is independent of acid inhibition. It is also a potent inhibitor of pancreatic function and growth of experimental tumors.

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)

The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.

A subclass of cyclooxygenase inhibitors with specificity for CYCLOOXYGENASE-2.

Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.

A 20-carbon unsaturated fatty acid containing 4 alkyne bonds. It inhibits the enzymatic conversion of arachidonic acid to prostaglandins E(2) and F(2a).

A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.

A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.

An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)

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).

A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.

A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.

That phase of a muscle twitch during which a muscle returns to a resting position.

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 neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.

The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.

A fetal blood vessel connecting the pulmonary artery with the descending aorta.

Analogs or derivatives of prostaglandins E that do not occur naturally in the body. They do not include the product of the chemical synthesis of hormonal PGE.

A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.

A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.

Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.

A group of LEUKOTRIENES; (LTC4; LTD4; and LTE4) that is the major mediator of BRONCHOCONSTRICTION; HYPERSENSITIVITY; and other allergic reactions. Earlier studies described a "slow-reacting substance of ANAPHYLAXIS" released from lung by cobra venom or after anaphylactic shock. The relationship between SRS-A leukotrienes was established by UV which showed the presence of the conjugated triene. (From Merck Index, 11th ed)

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.

An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.

A cyclooxygenase inhibiting, non-steroidal anti-inflammatory agent (NSAID) that is well established in treating rheumatoid arthritis and osteoarthritis and used for musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily.

A group of compounds that contain the structure SO2NH2.

The action of a drug that may affect the activity, metabolism, or toxicity of another drug.

Azoles of two nitrogens at the 1,2 positions, next to each other, in contrast with IMIDAZOLES in which they are at the 1,3 positions.

A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.

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.

Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.

Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)

A butyl-diphenyl-pyrazolidinedione that has anti-inflammatory, antipyretic, and analgesic activities. It has been used in ANKYLOSING SPONDYLITIS; RHEUMATOID ARTHRITIS; and REACTIVE ARTHRITIS.

An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.

An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2.

Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.

An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.

A non-steroidal anti-inflammatory agent that is less effective than equal doses of ASPIRIN in relieving pain and reducing fever. However, individuals who are hypersensitive to ASPIRIN may tolerate sodium salicylate. In general, this salicylate produces the same adverse reactions as ASPIRIN, but there is less occult gastrointestinal bleeding. (From AMA Drug Evaluations Annual, 1992, p120)

Drugs used to cause constriction of the blood vessels.

Drugs used to cause dilation of the blood vessels.

A class of compounds named after and generally derived from C20 fatty acids (EICOSANOIC ACIDS) that includes PROSTAGLANDINS; LEUKOTRIENES; THROMBOXANES, and HYDROXYEICOSATETRAENOIC ACIDS. They have hormone-like effects mediated by specialized receptors (RECEPTORS, EICOSANOID).

A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.

Arteries which arise from the abdominal aorta and distribute to most of the intestines.

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)

Substances that reduce or suppress INFLAMMATION.

A water-soluble extractive mixture of sulfated polysaccharides from RED ALGAE. Chief sources are the Irish moss CHONDRUS CRISPUS (Carrageen), and Gigartina stellata. It is used as a stabilizer, for suspending COCOA in chocolate manufacture, and to clarify BEVERAGES.

The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi.

The development of bony substance in normally soft structures.

The state of activity or tension of a muscle beyond that related to its physical properties, that is, its active resistance to stretch. In skeletal muscle, tonus is dependent upon efferent innervation. (Stedman, 25th ed)

A drug that has analgesic, anti-inflammatory, and antipyretic properties. It is the sodium sulfonate of AMINOPYRINE.

An enzyme of the oxidoreductase class primarily found in PLANTS. It catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives.

An anti-inflammatory analgesic and antipyretic of the phenylalkynoic acid series. It has been shown to reduce bone resorption in periodontal disease by inhibiting CARBONIC ANHYDRASE.

Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.

Medicated dosage forms that are designed to be inserted into the rectal, vaginal, or urethral orifice of the body for absorption. Generally, the active ingredients are packaged in dosage forms containing fatty bases such as cocoa butter, hydrogenated oil, or glycerogelatin that are solid at room temperature but melt or dissolve at body temperature.

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.

Pathological processes involving the STOMACH.

A non-steroidal anti-inflammatory agent with analgesic, anti-inflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase.

Drugs that prevent preterm labor and immature birth by suppressing uterine contractions (TOCOLYSIS). Agents used to delay premature uterine activity include magnesium sulfate, beta-mimetics, oxytocin antagonists, calcium channel inhibitors, and adrenergic beta-receptor agonists. The use of intravenous alcohol as a tocolytic is now obsolete.

A 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.

The nonstriated involuntary muscle tissue of blood vessels.

The flow of BLOOD through or around an organ or region of the body.

The salts or esters of salicylic acids, or salicylate esters of an organic acid. Some of these have analgesic, antipyretic, and anti-inflammatory activities by inhibiting prostaglandin synthesis.

The smallest divisions of the arteries located between the muscular arteries and the capillaries.

The glycine amide of 4-aminobenzoic acid. Its sodium salt is used as a diagnostic aid to measure effective renal plasma flow (ERPF) and excretory capacity.

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.

An essential amino acid that is physiologically active in the L-form.

A potent vasodilator agent that increases peripheral blood flow.

A lesion on the surface of the skin or a mucous surface, produced by the sloughing of inflammatory necrotic tissue.

A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.

Hydrochloric acid present in GASTRIC JUICE.

An anthranilic acid derivative with analgesic, anti-inflammatory, and antipyretic properties. It is used in musculoskeletal and joint disorders and administered by mouth and topically. (From Martindale, The Extra Pharmacopoeia, 30th ed, p16)

Pathological development in the JEJUNUM region of the SMALL INTESTINE.

The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)

Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.

Stimulation of renin release from rabbit renal cortex by arachidonic acid and prostaglandin endoperoxides. (1/4263)

The mechanism by which renal prostaglandins stimulate renin secretion in vivo is unknown. In this in vitro study we measured the effects of activation of the prostaglandin (PG) system on renin release from slices of rabbit renal cortex. The PG precursor arachidonic acid (C20:4), a natural PG endoperoxide (PGG2), two stable synthetic PG endoperoxide analogues (EPA I and II), PGE2, PGF2alpha, and two different PG synthesis inhibitors [indomethacin and 5,8,11,14-eicosatetraynoic acid (ETA)] were used to evaluate the possibility of a direct action of the cortical PG system on renin secretion. Renin release increased significantly with time after addition of C20:4, PGG2, EPA I, and EPA II to the incubation medium. Stimulation of renin release was se-related for C20:4 in concentrations of 0.6 to 4.5 X 10(-6) M, for EPA I in concentrations of 0.7 to 2.8 X 10(-6) M, and for EPA II in concentrations of 1.4 to 14.0 X 10(-6) M. Indomethacin (10(-4) M) and ETA (10(-4) M) significantly decreased basal renin release as well as the renin release stimulated by C20:4 and EPA I. PGE2(10(-12) to 10(-6) M) had no effect on renin release, whereas PGF2alpha (10(-12) to 10(-6) M) decreased renin release in a dose-dependent manner. These data raise the possibility of a direct action of the renal cortical PG system on renin secretion. The results further indicate that stimulation of renin release by C20:4 may depend more specifically on the action of PG endoperoxides than on the primary prostaglandins. (+info)

Non-steroidal anti-inflammatory drug-induced apoptosis in gastric cancer cells is blocked by protein kinase C activation through inhibition of c-myc. (2/4263)

Apoptosis plays a major role in gastrointestinal epithelial cell turnover, ulcerogenesis and tumorigenesis. We have examined apoptosis induction by non-steroidal anti-inflammatory drugs (NSAIDs) in human gastric (AGS) cancer cells and the role of protein kinase C (PKC) and apoptosis-related oncogenes. After treatment with aspirin or indomethacin, cell growth was quantified by MTT assay, and apoptosis was determined by acridine orange staining, DNA fragmentation and flow cytometry. The mRNA and protein of p53, p21waf1/cip1 and c-myc was detected by Northern and Western blotting respectively. The influence of PKC on indomethacin-induced apoptosis was determined by co-incubation of 12-O-tetradecanoylphorbol 13-acetate (TPA). The role of c-myc was determined using its antisense oligonucleotides. The results showed that both aspirin and indomethacin inhibited cell growth and induced apoptosis of AGS cells in a dose- and time-dependent manner, without altering the cell cycle. Indomethacin increased c-myc mRNA and protein, whereas p53 and p21wafl/cip1 were unchanged. Down-regulation of c-myc by its antisense oligonucleotides reduced apoptosis induction by indomethacin. TPA could inhibit indomethacin-induced apoptosis and accumulate cells in G2/M. Overexpression of c-myc was inhibited by TPA and p21waf1/cip1 mRNA increased. In conclusion, NSAIDs induce apoptosis in gastric cancer cells which may be mediated by up-regulation of c-myc proto-oncogene. PKC activation can abrogate the effects of NSAIDs by decreasing c-myc expression. (+info)

Anti-ulcer effects of 4'-(2-carboxyetyl) phenyl trans-4-aminomethyl cyclohexanecarboxylate hydrochloride (cetraxate) on various experimental gastric ulcers in rats. (3/4263)

Anti-ulcer effects of cetraxate, a new compound possessing anti-plasmin, anti-casein and anti-trypsin actions were investigated by using experimental gastric ulcer models in rats. Cetraxate, 300 mg/kg p.o. showed significant inhibitory effects of 65.3%, 70.0%, 30.2%, and 67.1% against aucte types of ulcers producing by aspirin, phenylbutazone, indomethacin, and pyloric ligature (Shay's ulcer), respectively. These effects were greater than those obtained by gefarnate and aluminum sucrose sulfate may be mainly attributed to the protecting action of this drug on gastric mucosa. Ctraxate further revealed remarkable inhibitory effects on chronic types of ulcers produced by acetic acid, clamping, and clamping-cortisone. In acetic acid ulcer in particular, cetraxate was found to have a dose-dependent inhibitory effect at doses over 50 mg/kg. Of test drugs including L-glutamine and methylmethionine sulfonium chloride, cetraxate showed the most remarkable inhibitory effect on beta-glucuronidase activity in ulcer tissue of these three types of ulcers. These findings suggest that cetraxate may prevent the connective tissue in the ulcer location from decomposition due to lysosomal enzymes such as beta-glucuronidase, thereby accelerating the recovery from ulcer. (+info)

Raf-1 is activated by the p38 mitogen-activated protein kinase inhibitor, SB203580. (4/4263)

SB203580 (4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imi dazole) is widely used as a specific inhibitor of p38 mitogen-activated protein kinase (MAPK). Here, we report that SB203580 activates the serine/threonine kinase Raf-1 in quiescent smooth muscle cells in a dose-dependent fashion. The concentrations of SB203580 required lie above those necessary to inhibit p38 MAPK and we were unable to detect basal levels of active p38 MAPK. SB203580 does not directly activate Raf-1 in vitro, and fails to activate Ras, MEK, and ERK in intact cells. In vitro, however, SB203580-stimulated Raf-1 activates MEK1 in a coupled assay. We conclude that activation of Raf-1 by SB203580 is not mediated by an inhibition of p38 MAPK, is Ras-independent, and is uncoupled from MEK/ERK signaling. (+info)

The cyclo-oxygenase-dependent regulation of rabbit vein contraction: evidence for a prostaglandin E2-mediated relaxation. (5/4263)

1. Arachidonic acid (0.01-1 microM) induced relaxation of precontracted rings of rabbit saphenous vein, which was counteracted by contraction at concentrations higher than 1 microM. Concentrations higher than 1 microM were required to induce dose-dependent contraction of vena cava and thoracic aorta from the same animals. 2. Pretreatment with a TP receptor antagonist (GR32191B or SQ29548, 3 microM) potentiated the relaxant effect in the saphenous vein, revealed a vasorelaxant component in the vena cava response and did not affect the response of the aorta. 3. Removal of the endothelium from the venous rings, caused a 10 fold rightward shift in the concentration-relaxation curves to arachidonic acid. Whether or not the endothelium was present, the arachidonic acid-induced relaxations were prevented by indomethacin (10 microM) pretreatment. 4. In the saphenous vein, PGE2 was respectively a 50 and 100 fold more potent relaxant prostaglandin than PGI2 and PGD2. Pretreatment with the EP4 receptor antagonist, AH23848B, shifted the concentration-relaxation curves of this tissue to arachidonic acid in a dose-dependent manner. 5. In the presence of 1 microM arachidonic acid, venous rings produced 8-10 fold more PGE2 than did aorta whereas 6keto-PGF1alpha and TXB2 productions remained comparable. 6. Intact rings of saphenous vein relaxed in response to A23187. Pretreatment with L-NAME (100 microM) or indomethacin (10 microM) reduced this response by 50% whereas concomitant pretreatment totally suppressed it. After endothelium removal, the remaining relaxing response to A23187 was prevented by indomethacin but not affected by L-NAME. 7. We conclude that stimulation of the cyclo-oxygenase pathway by arachidonic acid induced endothelium-dependent, PGE2/EP4 mediated relaxation of the rabbit saphenous vein. This process might participate in the A23187-induced relaxation of the saphenous vein and account for a relaxing component in the response of the vena cava to arachidonic acid. It was not observed in thoracic aorta because of the lack of a vasodilatory receptor and/or the poorer ability of this tissue than veins to produce PGE2. (+info)

Nitric oxide limits the eicosanoid-dependent bronchoconstriction and hypotension induced by endothelin-1 in the guinea-pig. (6/4263)

1. This study attempts to investigate if endogenous nitric oxide (NO) can modulate the eicosanoid-releasing properties of intravenously administered endothelin-1 (ET-1) in the pulmonary and circulatory systems in the guinea-pig. 2. The nitric oxide synthase blocker N(omega)-nitro-L-arginine methyl ester (L-NAME; 300 microM; 30 min infusion) potentiated, in an L-arginine sensitive fashion, the release of thromboxane A2 (TxA2) stimulated by ET-1, the selective ET(B) receptor agonist IRL 1620 (Suc-[Glu9,Ala11,15]-ET-1(8-21)) or bradykinin (BK) (5, 50 and 50 nM, respectively, 3 min infusion) in guinea-pig isolated and perfused lungs. 3. In anaesthetized and ventilated guinea-pigs intravenous injection of ET-1 (0.1-1.0 nmol kg(-1)), IRL 1620 (0.2-1.6 nmol kg(-1)), BK (1.0-10.0 nmol kg(-1)) or U 46619 (0.2-5.7 nmol kg(-1)) each induced dose-dependent increases in pulmonary insufflation pressure (PIP). Pretreatment with L-NAME (5 mg kg(-1)) did not change basal PIP, but increased, in L-arginine sensitive manner, the magnitude of the PIP increases (in both amplitude and duration) triggered by each of the peptides (at 0.25, 0.4 and 1.0 nmol kg(-1), respectively), without modifying bronchoconstriction caused by U 46619 (0.57 nmol kg(-1)). 4. The increases in PIP induced by ET-1, IRL 1620 (0.25 and 0.4 nmol kg(-1), respectively) or U 46619 (0.57 nmol kg(-1)) were accompanied by rapid and transient increases of mean arterial blood pressure (MAP). Pretreatment with L-NAME (5 mg kg(-1); i.v. raised basal MAP persistently and, under this condition, subsequent administration of ET-1 or IRL 1620, but not of U-46619, induced hypotensive responses which were prevented by pretreatment with the cyclo-oxygenase inhibitor indomethacin. 5. Thus, endogenous NO appears to modulate ET-1-induced bronchoconstriction and pressor effects in the guinea-pig by limiting the peptide's ability to induce, possibly via ET(B) receptors, the release of TxA2 in the lungs and of vasodilatory prostanoids in the systemic circulation. Furthermore, it would seem that these eicosanoid-dependent actions of ET-1 in the pulmonary system and on systemic arterial resistance in this species are physiologically dissociated. (+info)

Role of iNOS in the vasodilator responses induced by L-arginine in the middle cerebral artery from normotensive and hypertensive rats. (7/4263)

1. The substrate of nitric oxide synthase (NOS), L-arginine (L-Arg, 0.01 microM - 1 mM), induced endothelium-independent relaxations in segments of middle cerebral arteries (MCAs) from normotensive Wistar-Kyoto (WKY) and hypertensive rats (SHR) precontracted with prostaglandin F2alpha (PGF2alpha). These relaxations were higher in SHR than WKY arteries. 2. L-N(G)-nitroarginine methyl ester (L-NAME) and 2-amine-5,6-dihydro-6-methyl-4H-1,3-tiazine (AMT), unspecific and inducible NOS (iNOS) inhibitors, respectively, reduced those relaxations, specially in SHR. 3. Four- and seven-hours incubation with dexamethasone reduced the relaxations in MCAs from WKY and SHR, respectively. 4. Polymyxin B and calphostin C, protein kinase C (PKC) inhibitors, reduced the L-Arg-induced relaxation. 5. Lipopolysaccharide (LPS, 7 h incubation) unaltered and inhibited these relaxations in WKY and SHR segments, respectively. LPS antagonized the effect polymyxin B in WKY and potentiated L-Arg-induced relaxations in SHR in the presence of polymyxin B. 6. The contraction induced by PGF2alpha was greater in SHR than WKY arteries. This contraction was potentiated by dexamethasone and polymyxin B although the effect of polymyxin B was higher in SHR segments. LPS reduced that contraction and antagonized dexamethasone- and polymyxin B-induced potentiation, these effects being greater in arteries from SHR. 7. These results suggest that in MCAs: (1) the induction of iNOS participates in the L-Arg relaxation and modulates the contraction to PGF2alpha; (2) that induction is partially mediated by a PKC-dependent mechanism; and (3) the involvement of iNOS in such responses is greater in the hypertensive strain. (+info)

Effects of tumour necrosis factor-alpha on left ventricular function in the rat isolated perfused heart: possible mechanisms for a decline in cardiac function. (8/4263)

1. The cardiac depressant actions of TNF were investigated in the isolated perfused rat heart under constant flow (10 ml min(-1)) and constant pressure (70 mmHg) conditions, using a recirculating (50 ml) mode of perfusion. 2. Under constant flow conditions TNF (20 ng ml(-1)) caused an early (< 25 min) decrease in left ventricular developed pressure (LVDP), which was maintained for 90 min (LVDP after 90 min: control vs TNF; 110 +/- 4 vs 82 +/- 10 mmHg, P < 0.01). 3. The depression in cardiac function seen with TNF under constant flow conditions, was blocked by the ceramidase inhibitor N-oleoylethanolamine (NOE), 1 microM, (LVDP after 90 min: TNF vs TNF with NOE; 82 +/- 10 vs 11 +/- 5 mmHg, P < 0.05). 4. In hearts perfused at constant pressure, TNF caused a decrease in coronary flow rate (change in flow 20 min after TNF: control vs TNF; -3.0 +/- 0.9 vs -8.7 +/- 1.2 ml min(-1), P < 0.01). This was paralleled by a negative inotropic effect (change in LVDP 20 min after TNF: control vs TNF; -17 +/- 7 vs -46 +/- 6 mmHg, P < 0.01). The decline in function was more rapid and more severe than that seen under conditions of constant flow. 5. These data indicate that cardiac function can be disrupted by TNF on two levels, firstly via a direct, ceramidase dependant negative inotropic effect, and secondly via an indirect coronary vasoconstriction. (+info)

Patent ductus arteriosus (PDA) is a condition in which the DA fails to close after birth. This can result in excessive blood flow to the lungs and put extra strain on the heart. PDA is relatively common, occurring in about 1 in every 2000 live births.

Symptoms of PDA may include:

* Fast breathing (tachypnea)
* Shortness of breath (dyspnea)
* Fatigue
* Sweating during feedings
* Frequent respiratory infections

If left untreated, PDA can lead to long-term complications such as:

* Increased risk of respiratory infections
* Heart failure
* Developmental delays
* Cognitive impairments

Treatment for PDA may include:

* Medications to reduce blood pressure in the lungs and improve oxygenation
* Surgery to close the ductus arteriosus, either through a catheter or open-heart surgery

In some cases, PDA may be treated with medication alone. However, if the condition is not treated promptly, surgical intervention may be necessary to prevent long-term complications.

Stomach ulcers are caused by an imbalance between the acid and mucus in the stomach, which can lead to inflammation and damage to the stomach lining. Factors that can contribute to the development of a stomach ulcer include:

* Infection with the bacterium Helicobacter pylori (H. pylori)
* Overuse of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen
* Excessive alcohol consumption
* Smoking
* Stress
* Zollinger-Ellison syndrome, a rare condition that causes the stomach to produce too much acid.

Symptoms of a stomach ulcer may include:

* Pain in the upper abdomen, often described as a burning or gnawing sensation
* Nausea and vomiting
* Bloating and gas
* Abdominal tenderness
* Loss of appetite
* Weight loss

Treatment for stomach ulcers typically involves antibiotics to kill H. pylori, if present, and acid-suppressing medications to reduce the amount of acid in the stomach. In severe cases, surgery may be necessary. Lifestyle changes, such as avoiding NSAIDs, alcohol, and smoking, can also help manage symptoms and prevent recurrence.

Preventive measures for stomach ulcers include:

* Avoiding NSAIDs and other irritating substances
* Using acid-suppressing medications as needed
* Maintaining a healthy diet and lifestyle
* Managing stress
* Avoiding excessive alcohol consumption

It is important to seek medical attention if symptoms persist or worsen over time, as stomach ulcers can lead to complications such as bleeding, perforation, and obstruction. Early diagnosis and treatment can help prevent these complications and improve outcomes.

There are several types of edema, including:

1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.

Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.

Heterotopic ossification can cause a range of symptoms depending on its location and severity, including pain, stiffness, limited mobility, and difficulty moving the affected limb or joint. Treatment options for heterotopic ossification include medications to reduce inflammation and pain, physical therapy to maintain range of motion, and in severe cases, surgical removal of the abnormal bone growth.

In medical imaging, heterotopic ossification is often diagnosed using X-rays or other imaging techniques such as CT or MRI scans. These tests can help identify the presence of bone growth in an abnormal location and determine the extent of the condition.

Overall, heterotopic ossification is a relatively rare condition that can have a significant impact on a person's quality of life if left untreated. Prompt medical attention and appropriate treatment can help manage symptoms and prevent long-term complications.

There are many different types of stomach diseases, some of which include:

1. Gastritis: This is inflammation of the stomach lining, which can be caused by infection, autoimmune disorders, or excessive alcohol consumption.
2. Peptic ulcer: This is a sore on the lining of the stomach or duodenum (the first part of the small intestine). Peptic ulcers are often caused by infection with the bacterium Helicobacter pylori, but they can also be caused by excessive acid production.
3. Gastroesophageal reflux disease (GERD): This is a condition in which stomach acid flows back up into the esophagus, causing symptoms such as heartburn and difficulty swallowing.
4. Stomach cancer: This is a type of cancer that affects the stomach lining, and it can be caused by a variety of factors including age, diet, and family history.
5. Inflammatory bowel disease (IBD): This is a chronic condition that causes inflammation in the digestive tract, including the stomach. Crohn's disease and ulcerative colitis are examples of IBD.
6. Gastrointestinal motility disorders: These are conditions that affect the muscles and nerves of the digestive system, causing problems with movement and contraction of the stomach and intestines.
7. Stomach polyps: These are growths on the lining of the stomach that can be benign or cancerous.
8. Hiatal hernia: This is a condition in which part of the stomach bulges up into the chest through a hole in the diaphragm, which can cause symptoms such as heartburn and difficulty swallowing.
9. Gastroesophageal reflux disease (GERD): This is a chronic form of acid reflux that can cause symptoms such as heartburn and difficulty swallowing.
10. Zollinger-Ellison syndrome: This is a rare condition that causes the stomach to produce too much acid, leading to symptoms such as heartburn, nausea, and vomiting.

These are just some of the many possible causes of stomach pain. It's important to see a doctor if you experience persistent or severe stomach pain, especially if it is accompanied by other symptoms such as fever, bleeding, or difficulty swallowing. Your doctor can perform tests and examinations to determine the cause of your stomach pain and recommend appropriate treatment.

There are several types of ulcers, including:

1. Peptic ulcer: A type of ulcer that occurs in the lining of the stomach or duodenum (the first part of the small intestine). Peptic ulcers are caused by excess acid production and are often associated with stress, spicy foods, and certain medications.
2. Stomal ulcer: A type of ulcer that occurs in the stoma (the opening) of a surgically created ostomy (a procedure that creates an artificial opening in the abdominal wall).
3. Pressure ulcer: A type of ulcer that occurs as a result of prolonged pressure on the skin, often seen in people who are bedridden or have mobility issues.
4. Venous ulcer: A type of ulcer that occurs on the legs and is caused by poor blood flow and increased pressure in the veins.
5. Diabetic foot ulcer: A type of ulcer that occurs on the feet of people with diabetes, often as a result of nerve damage (neuropathy) and poor blood flow.

The symptoms of an ulcer can vary depending on its location and severity, but may include:

* Pain or discomfort in the affected area
* Redness and swelling around the ulcer
* Discharge or pus from the ulcer
* Fever or chills
* Difficulty healing

Treatment for an ulcer will depend on its cause and severity, but may include:

* Antibiotics to treat any underlying infections
* Medications to reduce acid production or protect the stomach lining
* Wound care and dressing changes to promote healing
* Surgery to close the ulcer or remove any dead tissue
* Changes to diet and lifestyle to manage underlying conditions such as diabetes or high blood pressure.

Here are some examples of jejunal diseases:

1. Crohn's disease: This is a chronic inflammatory bowel disease that can affect any part of the gastrointestinal tract, including the jejunum. It causes inflammation and damage to the lining of the intestine, leading to symptoms such as diarrhea, abdominal pain, and fatigue.
2. Ulcerative colitis: This is a chronic condition that causes inflammation and sores in the lining of the colon and rectum, but can also affect the jejunum. Symptoms include diarrhea, abdominal pain, and bloody stools.
3. Jejunoileal bypass surgery: This is a type of bariatric surgery that involves rerouting the small intestine to reduce the amount of food that can be absorbed. While it can lead to weight loss, it can also cause nutrient deficiencies and other complications.
4. Jejunal tumors: These are growths that can occur in the jejunum, which can be benign or malignant. Symptoms include abdominal pain, bloating, and obstruction of the intestine.
5. Jejunal strictures: These are narrowing of the jejunum that can cause obstruction of food passage and lead to symptoms such as abdominal pain, nausea, and vomiting.
6. Jejunal inflammatory fibrosis: This is a condition where the jejunum becomes inflamed and scarred, leading to thickening of the intestinal walls and narrowing of the intestine. Symptoms include abdominal pain, diarrhea, and malabsorption.
7. Jejunal enteropathy: This is a condition where the jejunum becomes damaged, leading to symptoms such as diarrhea, abdominal pain, and weight loss. It can be caused by a variety of factors, including infection, inflammation, and autoimmune disorders.
8. Jejunal ulcers: These are open sores that can occur in the lining of the jejunum, often as a result of infection or inflammation. Symptoms include abdominal pain, nausea, and vomiting.
9. Jejunal ischemia: This is a condition where the blood supply to the jejunum is reduced, leading to damage to the intestinal tissue. Symptoms include abdominal pain, diarrhea, and rectal bleeding.
10. Jejunal cancer: This is a rare type of cancer that can occur in the jejunum. Symptoms include abdominal pain, weight loss, and rectal bleeding.

These are just a few examples of the many different conditions that can affect the jejunum. If you suspect that you or someone you know may have a condition affecting the jejunum, it is important to seek medical attention as soon as possible for proper diagnosis and treatment.

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with P. L. Boardman: Hart FD, Boardman PL (27 November 1965). "Indomethacin and phenylbutazone: a comparison". Br Med J. 2 ( ... Hart, F. Dudley; Boardman, P. L. (19 October 1963). "Indomethacin: A New Non-steroid Anti-inflammatory Agent". BMJ. 2 (5363): ...

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Johnston PG, Gillam-Krakauer M, Fuller MP, Reese J (March 2012). "Evidence-based use of indomethacin and ibuprofen in the ... "Arthrexin Indomethacin PRODUCT INFORMATION" (PDF). TGA eBusiness Services. Alphapharm Pty Limited. 14 October 2011. Archived ... Neumann R, Schulzke SM, Bührer C (2012). "Oral ibuprofen versus intravenous ibuprofen or intravenous indomethacin for the ...

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Only indomethacin (brand name Indocin) has been studied with respect to relief of pleurisy. Codeine-based cough syrups to ... Non-steroidal anti-inflammatory drugs (NSAIDs), preferably indometacin, are usually employed as pain control agents. A number ... Klein RC (October 1984). "Effects of indomethacin on pleural pain". South. Med. J. 77 (10): 1253-4. doi:10.1097/00007611- ...

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NSAIDs (such as indomethacin) and calcium channel blockers (such as nifedipine) are the most likely to delay delivery for 48 ... "Indomethacin Side Effects: Common, Severe, Long Term". Drugs.com. Retrieved 30 July 2021. Management of high-risk pregnancy : a ... The efficacy of β-adrenergic agonists, atosiban, and indomethacin is a decreased odds ratio (OR) of delivery within 24 hours of ... Macones, George A.; Robinson, Charlah A. (1997). "Is there justification for using indomethacin in preterm labor? An analysis ...

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It may be less nephrotoxic than indomethacin. There are two known polymorphs of the compound. Nabumetone has little effect on ... a comparison of indomethacin and nabumetone". Clinical Science. 97 (4): 457-465. doi:10.1042/cs0970457. PMID 10491346. S2CID ...

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Indomethacin in a study by Blanchard et al. 2015 was shown to increase serum potassium levels, and decrease renin concentration ... In patients with early onset of the disease such as infants and children, indomethacin is the drug of choice utilized to treat ... Adverse effects of indomethacin include a decrease in the glomerular filtration rate, and gastrointestinal disturbances. ... February 2015). "Indomethacin, amiloride, or eplerenone for treating hypokalemia in Gitelman syndrome". Journal of the American ...

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... enhanced bioavailability of indomethacin". Journal of Controlled Release. 90 (3): 335-43. doi:10.1016/s0168-3659(03)00200-1. ...

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Two patients with an absolute response to indomethacin". Cephalalgia. 30 (6): 757-760. doi:10.1111/j.1468-2982.2009.02003.x. ...

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... enhanced bioavailability of indomethacin". Journal of Controlled Release. 90 (3): 335-43. doi:10.1016/S0168-3659(03)00200-1. ...

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In one study, indomethacin, 150 mg per day, was given for the first week, and 100 mg per day was given for 2 additional weeks. ... No patient had a relapse after discontinuation of indomethacin. Other alternatives to corticosteroid treatment include dapsone ...

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Ferreira; Moncada, S; Vane, JR (1971). "Indomethacin and aspirin abolish prostaglandin release from the spleen". Nature New ...

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Almost all cases of CPH respond positively and effectively to indometacin, but as much as 25 percent of patients discontinued ... CPH headaches are treated through the use of non-steroidal anti-inflammatory drugs, with indomethacin found to be usually ... CPH affects all over the head Individuals with CPH are far more responsive to indomethacin than individuals with cluster ... found that all patients diagnosed with CPH were responsive to indomethacin and were able to completely control their symptoms. ...

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... to treatment with the anti-inflammatory drug indomethacin where in most cases CH typically shows no positive indomethacin ... Prakash, Sanjay; Shah, Nilima D; Chavda, Bhavna V (2010). "Cluster headache responsive to indomethacin: Case reports and a ... Sanjay Prakash, Nilima D Shah, Bhavna V Chavda (2010). "Cluster headache responsive to indomethacin: Case reports and a ... Sjaastad, O; Vincent, M (2010). "Indomethacin responsive headache syndromes: Chronic paroxysmal hemicrania and Hemicrania ...

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Tamaoki J, Chiyotani A, Kobayashi K, Sakai N, Kanemura T, Takizawa T (1992). "Effect of indomethacin on bronchorrhea in ... Tamaoki J, Kohri K, Isono K, Nagai A (2000). "Inhaled indomethacin in bronchorrhea in bronchioloalveolar carcinoma: role of ... "Successful treatment of refractory bronchorrhea by inhaled indomethacin in two patients with bronchioloalveolar carcinoma". ... epidermal growth factor receptor tyrosine kinase inhibitor indomethacin corticosteroids octreotide radiation therapy ...

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with L. P. J. Holt: Holt, L. P. J.; Hawkins, C. F. (22 May 1965). "Indomethacin: studies of absorption and of the use of ... indomethacin suppositories". Br Med J. 1 (5446): 1354-1356. doi:10.1136/bmj.1.5446.1354. PMC 2165800. PMID 14278842. Hawkins, C ...

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Indomethacin has been associated with rare cases of idiosyncratic drug induced liver disease. ... Indomethacin is a potent nonsteroidal antiinflammatory drug (NSAID) typically used for chronic inflammatory arthritis. ... Side-effects of indomethacin. Ann Rheum Dis 1967; 26: 127-32. (Discussion of side effects of indomethacin based upon results in ... Indomethacin No authors listed In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. ...

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... or oral indomethacin [‎3 x 0.2 mg/kg at 24-hour intervals]‎. Complete ductal closure was seen in 7/10 of the indomethacin and 8 ... Pourarian, Sh., Pishva, N., Madani, A. & Rastegari, M. (‎2008)‎. Comparison of oral ibuprofen and indomethacin on closure of ... Although intravenous indomethacin and ibuprofen are widely used for closure of patent ductus arteriosus in premature infants, ... Comparison of oral ibuprofen and indomethacin on closure of patent ductus arteriosus in preterm infants. ...

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doi: 10.1007/s11910-014-0516-y. Indomethacin-responsive headaches. VanderPluym J1. Author information Abstract ... New research 888: Indomethacin-responsive headaches. Curr Neurol Neurosci Rep. 2015 Feb;15(2):516. doi: 10.1007/s11910-014-0516 ... These "novel" indomethacin-responsive headaches beg the question of what headache characteristics are required to qualify a ... Indomethacin-responsive headaches are a heterogeneous group of primary headache disorders distinguished by their swift and ...

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Although intravenous indomethacin and ibuprofen are widely used for closure of patent ductus arteriosus in premature infants, these formulations are unavailable in the Islamic Republic of Iran. (who.int)
Intravenous indometacin is administered to close a hemodynamically significant patent ductus arteriosus, as indicated by clinical evidence, in premature infants. (rcsb.org)
A177871,L6778] Intravenous indometacin is indicated to induce closure of a hemodynamically significant patent ductus arteriosus in premature infants weighing between 500 and 1750 g when after 48 hours usual medical management (e.g., fluid restriction, diuretics, digitalis, respiratory support, etc.) is ineffective. (rcsb.org)

Limit use of NSAIDs, including indomethacin capsules, between about 20 to 30 weeks in pregnancy due to the risk of oligohydramnios/fetal renal dysfunction. (nih.gov)
anti-inflammatory drugs (NSAIDs) such as ibuprofen or indomethacin when symptoms begin. (nih.gov)
A177871] Since then, indometacin has been extensively studied in clinical trials as one of the most potent NSAIDs in blocking prostaglandin synthesis and was among the first NSAIDs to be used in the symptomatic treatment of migraine and for headaches that eventually became known as "indomethacin-responsive" headache disorders. (rcsb.org)
Indomethacin belongs to a class of non-steroidal anti-inflammatory drugs (NSAIDs). (buycialisonliney.com)
To test the hypothesis that non-steroidal anti-inflammatory drugs (NSAIDs) accelerate the progression of osteoarthritis by reducing synthesis of vasodilator prostaglandins, thereby diminishing joint perfusion, 105 osteoarthritis patients awaiting hip arthroplasty were treated prospectively with a strong or weak prostaglandin synthesis inhibitor, indomethacin or azapropazone, respectively. (nih.gov)
Some people may not be able to tolerate long-term use of indomethacin and may have to rely on less effective NSAIDs. (nih.gov)

Indomethacin is a type of nonsteroidal anti-inflammatory drug. (medlineplus.gov)

A177871] The pharmacological effect of indometacin is not fully understood, however, it is thought to be mediated through potent and nonselective inhibition of the enzyme cyclooxygenase (COX), which is the main enzyme responsible for catalyzes the rate-limiting step in prostaglandin and thromboxane biosynthesis via the arachidonic acid (AA) pathway. (rcsb.org)
Therefore, we examined the involvement of prostaglandin in experimentally induced ARDS by using prostaglandin synthesis inhibitor, indomethacin. (who.int)

Relationships between the concentrations of prostaglandins and the nonsteroidal antiinflammatory drugs indomethacin, diclofenac, and ibuprofen. (nih.gov)
Indomethacin inhibits the production of prostaglandins and relieve the pain and inflammation. (dd-database.org)
The patients receiving azapropazone, who had higher concentrations of synovial vasodilator prostaglandins, took longer than the indomethacin group to reach the arthroplasty end-point. (nih.gov)

and moderate to severe osteoarthritis is indomethacin capsules 25 mg two or three times a day. (nih.gov)
A177871] Most commonly used in rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, acute shoulder pains, and acute gouty arthritis, indometacin is currently available as oral capsules as well as other methods of administration, including rectal and intravenous formulations. (rcsb.org)
Oral indometacin is indicated for symptomatic management of moderate to severe rheumatoid arthritis including acute flares of chronic disease, moderate to severe ankylosing spondylitis, moderate to severe osteoarthritis, acute painful shoulder (bursitis and/or tendinitis) and acute gouty arthritis. (rcsb.org)

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In this study of the therapeutic effects of oral treatments, 20 preterm infants were randomized to oral ibuprofen (1 × 10 mg/kg, then 2 × 5 mg/kg at 24-hour intervals) or oral indomethacin (3 × 0.2 mg/kg at 24-hour intervals). (who.int)

The trial was divided into two groups (n=64) using a randomised number table group A will be given 100 mg of indomethacin suppository rectally and group B will be given 8 mg of intravenous lornoxicam. (bvsalud.org)

March 4 issue),* very early treatment with indomethacin was shown to prevent the development of a hemodynamically important shunt through the ductus arteriosus among newborn infants weighing less than 1000 g at birth. (elsevierpure.com)
One of the important benefits to the indomethacin-treated infants but not to those receiving a placebo was a statistically significant shorter time needed to regain birth weight. (elsevierpure.com)
Three of the 12 infants who received placebo had necrotizing enterocolitis, but none of the 10 infants given indomethacin had this problem. (elsevierpure.com)

The dosage for acute gouty arthritis is indomethacin capsules 50 mg three times a day. (nih.gov)
Indomethacin is a potent nonsteroidal antiinflammatory drug (NSAID) typically used for chronic inflammatory arthritis. (nih.gov)
Sudden death of a child with juvenile chronic arthritis, probably due to indomethacin. (nih.gov)
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Indomethacin overdose occurs when someone takes more than the normal or recommended amount of this medicine. (medlineplus.gov)
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On the eye, indomethacin is used to treat inflammation of the front section of the eye after surgery. (dd-database.org)
L10553] Ophthalmic indometacin has been studied and used in the symptomatic treatment of postoperative ocular inflammation and pain and/or complications after cataract surgery. (rcsb.org)
Value of indomethacin suppository for preoperative analgesia and anti-inflammation in laparoscopic appendectomy: a protocol of prospective, double-blinded, single-centre, randomised controlled trial in China. (bvsalud.org)

We have developed a valid predictive model for predicting SIVH as well as shown that exposure to indomethacin decreases the incidence of SIVH overall. (elsevier.com)

These highlights do not include all the information needed to use INDOMETHACIN CAPSULES safely and effectively. (nih.gov)
See full prescribing information for INDOMETHACIN CAPSULES. (nih.gov)
Avoid use of indomethacin capsules in patients with severe heart failure unless benefits are expected to outweigh risk of worsening heart failure. (nih.gov)
Indomethacin capsules are contraindicated in patients with aspirin-sensitive asthma. (nih.gov)
Discontinue indomethacin capsules at first appearance of skin rash or other signs of hypersensitivity. (nih.gov)

In fact, gout patients treated with Celecoxib have the same treatment response as Indomethacin. (nbmeanswers.com)
Indomethacin is typically the DOC, better than celecoxib. (nbmeanswers.com)
Higher doses of celecoxib are needed to reach similar pain relief in acute gout compared to indomethacin. (nbmeanswers.com)

In addition, indomethacin and atorvastatin ameliorated abnormal cytokine secretion, lymphocyte subset disorder, and hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axis imbalances in APP/PS1 mice. (nih.gov)

Diclofenac es metabolizado por el hígado y excretado por vía biliar y renal, principalmente como metabolitos en forma de glucuronatos o sulfatos. (artistrydance.hu)

abstract = "Prophylactic indomethacin may decrease Severe Intraventricular Hemorrhage (SIVH). (elsevier.com)

Two other human proteins-PGES-2 and SIGMAR1-were of particular interest because they are targets of existing drugs, including the anti-inflammatory indomethacin for PGES-2 and antipsychotics like haloperidol for SIGMAR1. (nih.gov)
Nonsteroidal anti-inflammatory drugs (including indomethacin) may rarely increase the risk for a heart attack or stroke. (healthwarehouse.com)
Read also the information about the drug group non-steroidal anti-inflammatory drugs, to which belongs the active ingredient indomethacin. (dd-database.org)
Indomethacin works like the other nonsteroidal anti-inflammatory drugs from subgroup of acetic acid compounds. (dd-database.org)

Below are symptoms of an indomethacin overdose in different parts of the body. (medlineplus.gov)
Indomethacin provides rapid relief from symptoms. (nih.gov)

jaypat Indomethacin is typically the first choice NSAID for acute gout flares. (nbmeanswers.com)
IMSEAR at SEARO: Indomethacin Exacerbates Oleic Acid-Induced Acute Respiratory Distress Syndrome in Adult Rats. (who.int)

The simultaneous ingestion of indomethacin and digoxin, lithium, methotrexate, or phenytoin increases the concentration of those substances in the blood. (dd-database.org)
6. Enhancement of etoposide and methotrexate sensitivity by indomethacin in vitro. (nih.gov)

Indomethacin-responsive headaches are a heterogeneous group of primary headache disorders distinguished by their swift and often absolute response to indomethacin. (ouchuk.org)
Case reports of other primary headache disorders that also respond to indomethacin, such as cluster headache, nummular headache, and ophthalmoplegic migraine, have been described. (ouchuk.org)

For example, flare up are at of involvement potential to typically develop may require are how Do I Buy Indomethacin by a. (totoscleaning.com)

Traditionally, indomethacin-responsive headaches include a subset of trigeminal autonomic cephalalgias (paroxysmal hemicrania and hemicrania continua), Valsalva-induced headaches (cough headache, exercise headache, and sex headache), primary stabbing headache, and hypnic headache. (ouchuk.org)

Indomethacin-responsive headaches. (ouchuk.org)
These "novel" indomethacin-responsive headaches beg the question of what headache characteristics are required to qualify a headache as an indomethacin-responsive headache. (ouchuk.org)

Read the Medication Guide provided by your pharmacist before you start using indomethacin and each time you get a refill. (healthwarehouse.com)

How well someone does depends on how much indomethacin was swallowed and how quickly treatment is received. (medlineplus.gov)
They found that COVID-19 patients taking indomethacin were less likely than those taking an anti-inflammatory that doesn't target PGES-2 to require treatment at a hospital. (nih.gov)
Treatment with indomethacin and atorvastatin ameliorated impairments in spatial learning and memory, and the active avoidance response in APP/PS1 mice. (nih.gov)
The headache must also be completely responsive to treatment with the non-steroidal anti-inflammatory drug (NSAID) indomethacin. (nih.gov)

These headache syndromes differ in extent of response to indomethacin, clinical features, and differential diagnoses. (ouchuk.org)

More analysis shows that the volume as well as the surface area of the micelle expand significantly in the presence of indomethacin, and are fairly the same in the presence of ibuprofen. (aps.org)
Pulmonary water content in indomethacin pretreated animals was also significantly greater than control group. (who.int)

Application of the model to patients receiving indomethacin suggests a benefit at the highest risk levels. (elsevier.com)

Indomethacin is used mostly for pain due to joint diseases. (dd-database.org)
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In the indomethacin group the affected hips lost joint space more rapidly than did the contralateral hips, a difference not seen in the azapropazone group. (nih.gov)

The pain, which covers indomethacin here, range from mild to moderately severe pain or of strong to very severe pain. (dd-database.org)

Complete ductal closure was seen in 7/10 of the indomethacin and 8/10 of the ibuprofen group. (who.int)

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Known hypersensitivity to indomethacin or any components of the drug product. (nih.gov)
Indomethacin has been associated with rare cases of idiosyncratic drug induced liver disease. (nih.gov)
Indometacin, or indomethacin, is a non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic, and antipyretic properties. (rcsb.org)
The non-steroidal anti-inflammatory drug indomethacin suppository has antipyretic and analgesic effects. (bvsalud.org)

Anatomy10

Organisms6

Diseases7

Chemicals and Drugs71

Phenomena and Processes8

Stimulation of renin release from rabbit renal cortex by arachidonic acid and prostaglandin endoperoxides. (1/4263)

Non-steroidal anti-inflammatory drug-induced apoptosis in gastric cancer cells is blocked by protein kinase C activation through inhibition of c-myc. (2/4263)

Anti-ulcer effects of 4'-(2-carboxyetyl) phenyl trans-4-aminomethyl cyclohexanecarboxylate hydrochloride (cetraxate) on various experimental gastric ulcers in rats. (3/4263)

Raf-1 is activated by the p38 mitogen-activated protein kinase inhibitor, SB203580. (4/4263)

The cyclo-oxygenase-dependent regulation of rabbit vein contraction: evidence for a prostaglandin E2-mediated relaxation. (5/4263)

Nitric oxide limits the eicosanoid-dependent bronchoconstriction and hypotension induced by endothelin-1 in the guinea-pig. (6/4263)

Role of iNOS in the vasodilator responses induced by L-arginine in the middle cerebral artery from normotensive and hypertensive rats. (7/4263)

Effects of tumour necrosis factor-alpha on left ventricular function in the rat isolated perfused heart: possible mechanisms for a decline in cardiac function. (8/4263)

Indomethacin

Cyclooxygenase Inhibitors

Prostaglandins

Anti-Inflammatory Agents, Non-Steroidal

Dinoprostone

Prostaglandins E

Prostaglandin-Endoperoxide Synthases

Prostaglandin Antagonists

Ductus Arteriosus, Patent

Cyclooxygenase 1

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyrazol-3-amine

Stomach Ulcer

Arachidonic Acids

Ibuprofen

Gastric Mucosa

6-Ketoprostaglandin F1 alpha

Masoprocol

Meclofenamic Acid

Arachidonic Acid

Prostaglandins F

Dose-Response Relationship, Drug

Epoprostenol

Cyclooxygenase 2

Lipoxygenase Inhibitors

Bradykinin

16,16-Dimethylprostaglandin E2

Aspirin

Vasodilation

Cyclooxygenase 2 Inhibitors

Biological Factors

Nitrobenzenes

5,8,11,14-Eicosatetraynoic Acid

Nitric Oxide

NG-Nitroarginine Methyl Ester

Nitroarginine

Thromboxane B2

Rats, Wistar

Guinea Pigs

Muscle Relaxation

Thromboxane A2

Acetylcholine

Vasoconstriction

Ductus Arteriosus

Prostaglandins E, Synthetic

Dinoprost

Rats, Inbred Strains

Muscle Contraction

Endothelium, Vascular

SRS-A

Rabbits

Histamine

Piroxicam

Sulfonamides

Drug Interactions

Pyrazoles

Rats, Sprague-Dawley

Thromboxanes

Edema

Muscle, Smooth

Phenylbutazone

Nitric Oxide Synthase

Quinacrine

Enzyme Inhibitors

Ketoprofen

Sodium Salicylate

Vasoconstrictor Agents

Vasodilator Agents

Butanones

Eicosanoids

Diclofenac

Mesenteric Arteries

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid

Anti-Inflammatory Agents

Carrageenan

Trachea

Ossification, Heterotopic

Muscle Tonus

Dipyrone

Lipoxygenase

Flurbiprofen