prostaglandin/infarction

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Plasma 8-iso-prostaglandin F2alpha, a marker of oxidative stress, is increased in patients with acute myocardial infarction.

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BACKGROUND Oxidative stress has been implicated in the pathogenesis of atherogenesis. The aim of our study is to examine whether the plasma 8-iso-prostaglandin F(2alpha) level, a marker of oxidative stress, is elevated in patients with acute myocardial infarction. METHODS Three groups of patients

Antimuscarinics suppress adenosine triphosphate and prostaglandin E2 release from urothelium with potential improvement in detrusor overactivity in rats with cerebral infarction.

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OBJECTIVE Antimuscarinics improve detrusor overactivity. We evaluated the effects and action mechanisms of imidafenacin (Kyorin Pharmaceutical, Tokyo, Japan), a novel therapeutic agent for overactive bladder with antimuscarinic activity, on mediator release from urothelium and detrusor overactivity

Randomized trial of ridogrel, a combined thromboxane A2 synthase inhibitor and thromboxane A2/prostaglandin endoperoxide receptor antagonist, versus aspirin as adjunct to thrombolysis in patients with acute myocardial infarction. The Ridogrel Versus Aspirin Patency Trial (RAPT).

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BACKGROUND Aspirin, by nonselectively blocking cyclooxygenase both in platelets and in endothelial cells, not only inhibits the thromboxane A2 pathway of platelet activation but at the same time also the generation of vasodilating and platelet-inhibitory prostanoids, such as prostacyclin, by the

Reduction by prostaglandin E1 or prostaglandin E0 of myocardial infarct size in the rabbit by activation of ATP-sensitive potassium channels.

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1. This study examined whether pretreatment of rabbits with infusions of prostaglandin E1 (PGE1) or prostaglandin E0 (PGE0) (which were terminated prior to the onset of ischaemia) reduce myocardial infarct size arising from coronary artery occlusion (60 min) and reperfusion (120 min). In addition,

Increased platelet thromboxane A2/prostaglandin H2 receptors in patients with acute myocardial infarction.

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Platelets have been implicated in the formation of occlusive intracoronary thrombi leading to unstable angina pectoris and acute myocardial infarction. Evidence of platelet involvement in these syndromes includes increased thromboxane A2 synthesis during ischemic events and enhanced in vitro

Intracoronary prostaglandin E1 plus streptokinase in acute myocardial infarction.

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Fourteen patients with acute myocardial infarction (duration of chest pain 5 +/- 2 hours) received intracoronary infusion of prostaglandin E1 (PGE1) and streptokinase. Intracoronary PGE1 was followed by intracoronary streptokinase in 10 patients (group A), with successful recanalization in all

Transcardiac 8-iso-prostaglandin F(2 alpha)generation from acute myocardial infarction heart: insight into abrupt reperfusion and oxidant stress.

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8-iso-prostaglandin F(2 alpha)(8-iso-PGF(2 alpha)), a representative isoprostane, has been reported to be a reliable marker for oxidant stress in vivo. To examine if 8-iso-PGF(2 alpha)is generated in patients with acute myocardial infarction (AMI), we measured the level of immunoreactive 8-iso PGF(2

Effect of aspirin on renal function and the prostaglandin-kallikrein systems early after myocardial infarction.

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Using a double-blind procedure, 29 patients with a recent myocardial infarction were randomly allocated to a placebo group (n = 14) and to a group receiving aspirin, 300 mg three times a day (n = 15) over 7 days. No change in renal function was observed in either treatment group. Compared with the

Reduction of canine infarct size by bolus intravenous administration of liposomal prostaglandin E1: comparison with control, placebo liposomes, and continuous intravenous infusion of prostaglandin E1.

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Prostaglandin E1 (PGE1) reduces experimental infarct size when administered by prolonged low-dose left atrial infusion during coronary occlusion. Liposomal delivery of PGE1 may enhance biologic activity and limit adverse hemodynamic effects. The purpose of this study was to test the hypothesis that

[Primary prostaglandins PGE2, PGF2, prostacyclin and thromboxane in patients with myocardial infarction].

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In 47 patients with acute myocardial infarction and in 17 healthy volunteers blood concentration and urinary excretion of PGE2, PGF2 alpha, 6-keto-PGF1 alpha--hydrolysis product of prostacyclin--and TXB2 were determined using RIA. Myocardial infarction patients were found to have significantly

Effects of endogenously produced leukotrienes, thromboxane, and prostaglandins on coronary vascular resistance in rabbit myocardial infarction.

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In an effort to evaluate the synthesis and function of eicosanoids in myocardial infarction, we have developed a technique of in vivo myocardial infarction in rabbits followed by ex vivo cardiac perfusion. Isolated Langendorff perfused infarcted hearts (removed 1 or 4 d after infarction) responded

Infarct salvage with liposomal prostaglandin E1 administered by intravenous bolus immediately before reperfusion in a canine infarction-reperfusion model.

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BACKGROUND Prostaglandin E1 (PGE1) inhibits leukocyte and platelet function and reduces infarct size during left atrial infusion. Intravenous liposomal PGE1 (TLC C-53) accelerates thrombolysis and prevents reocclusion in canine coronary thrombosis. We tested the hypothesis that intravenous TLC C-53

Reduction of experimental canine myocardial infarct size with prostaglandin E1: inhibition of neutrophil migration and activation.

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The ability of prostaglandin E1 (PGE1) to reduce myocardial infarct size in an anesthetized open-chest canine model of regional myocardial ischemia and reperfusion was investigated. Administration of PGE1 (100 ng/kg/min into the left atrium) to dogs beginning 10 min after left circumflex coronary

Hemodynamic effects of prostaglandin E1 infusion in patients with acute myocardial infarction and left ventricular failure.

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Prostaglandin E1 (PGE1) has been shown to limit infarct size, improve coronary blood flow, inhibit platelet aggregation, and reduce both left ventricular (LV) preload and afterload in experimental animals. Its use in the therapy of patients with acute myocardial infarction (AMI) and congestive heart

Microsomal prostaglandin E2 synthase-1 deletion leads to adverse left ventricular remodeling after myocardial infarction.

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BACKGROUND Pharmacological inhibition of cyclooxygenase-2 increases the risk of myocardial infarction (MI) and stroke. Microsomal prostaglandin (PG) E(2) synthase-1 (mPGES-1), encoded by the Ptges gene, functions downstream from cyclooxygenase-2 in the inducible PGE(2) biosynthetic pathway. We

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