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Sida 1 från 32 resultat
Effects of energostim on the sympathoadrenal system and contents of pyridine nucleotides during acute myocardial infarction.
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The contents of myofibrillar creatine phosphokinase and cytochrome c, the key enzyme of the mitochondrial respiratory chain, increased, while the content of nicotinamide coenzymes and redox potential (NAD/NADH ratio) sharply decreased over the first 6 h of acute myocardial infarction. The contents
Octahydrocyclopenta[c]pyridine and octahydrocyclopenta[c]pyran analogues as a protease activated receptor 1 (PAR1) antagonist.
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Protease activated receptor 1 (PAR1) has been considered as a promising antiplatelet target to prevent thrombotic cardiovascular events in patients with prior myocardial infarction or peripheral arterial diseases. Previously, we found a series of octahydroindene analogues to have high potency on
Protective effect of the new antiplatelet agent 2-methyl-3-(1,4,5,6-tetrahydronicotinoyl)pyrazolo[1,5-a]pyridine on myocardial damage due to coronary occlusion and reperfusion in rabbit.
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The effects of KC-764 (2-methyl-3-(1,4,5,6-tetrahydronicotinoyl)pyrazolo[1,5-a]pyridine, CAS 94457-09-7) on infarct size, myeloperoxidase (MPO) activity and plasma prostanoid levels were studied using coronary artery occlusion (1 h)-reperfusion (3 h) model in rabbits, comparing with acetylsalicylic
Regression of hypertrophy after myocardial infarction is produced by the chronic blockade of angiotensin type 1 receptor in rats.
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The efficacy of angiotensin converting enzyme (ACE) inhibitors is well known to prevent the formation of angiotensin II (Ang II) by these agents. The objective of the present study was to evaluate the hemodynamic, biochemical, and morphological responses to Ang II receptor blockade with E-4177,
-(S)-Alpha-phenyl-2-pyridine-ethanamine Dihydrochloride-, a low affinity uncompetitive N-methyl-D-aspartic acid antagonist, is effective in rodent models of global and focal ischemia.
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[(S)-Alpha-phenyl-2-pyridine-ethanamine dihydrochloride] (ARL 15896AR) is a low affinity uncompetitive N-methyl-D-aspartic acid receptor antagonist that was tested in animal models of anoxia and ischemia. Pretreatment of rodents with ARL 15896AR extended survival time during exposure to hypoxia.
[Effect of KC-404 on experimental cerebral infarction in rats].
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Experimental cerebral infarction accompanying altered cerebral energy metabolism and cerebral edema was produced in rats by injecting arachidonate into the left carotid artery. In the present study, the effects of 3-isobutyryl-2-isopropylpyrazolo [1,5-alpha]pyridine (KC-404) on these ischemic
Effects of a pyridine derivative thromboxane synthetase inhibitor and its inactive isomer in endotoxic shock in the rat.
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1 We investigated the effects of a pyridine derivative thromboxane synthetase inhibitor and its inactive ortho isomer on arachidonic acid metabolism and pathophysiological sequelae of endotoxic shock. In vehicle-treated rats, 30 min after intravenous S. enteritidis endotoxin (15 mg/kg), plasma iTxB2
Effects of the calcium antagonist AE0047 on the development of neurological deficit and infarction after middle cerebral artery occlusion in stroke-prone spontaneously hypertensive rats.
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AE0047 [4-(4-benzhydrylpiperazino)phenethyl methyl 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridine dicarboxylate dihydrochloride] is a new dihydropyridine calcium antagonist with protective effects against cerebral ischaemia and the occurrence of stroke in several animal models. We
Influence on hemodynamic parameters after parenteral administration of AR-L 115 BS in patients with acute myocardial infarction.
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2-[(2-Methoxy-4-methylsulfinyl)phenyl]-1H-imidazo [4,5-b]pyridine (AR-L 115 BS) in a single dosage of 0.75 mg/kg body weight was given i.v. to 8 patients with acute myocardial infarction confirmed clinically, electrocardiographically and enzymatically. Hemodynamic measurements were performed before
A facile synthesis of new 2-carboxamido-3-carboxythiophene and 4,5,6,7-tetrahydro-2-carboxamido-3-carboxythieno[2,3-c]pyridine derivatives as potential endothelin receptors ligands.
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Endothelins (ETs) are the most ubiquitous, highly potent and unusually long-lasting peptidic constrictors of human vessels known. Elevated levels of the plasma concentration of ETs were observed in several diseases such as hypertension, acute myocardial infarction, congestive heart failure, renal
Discovery of 3,3'-(2,4-diaminopteridine-6,7-diyl)diphenol as an isozyme-selective inhibitor of PI3K for the treatment of ischemia reperfusion injury associated with myocardial infarction.
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In studies aimed toward identifying effective and safe inhibitors of kinase signaling cascades that underlie ischemia/reperfusion (I/R) injury, we synthesized a series of pteridines and pyridopyrazines. The design strategy was inspired by the examination of naturally occurring PI3K inhibitors such
Genetic deletion of CD38 confers post-ischemic myocardial protection through preserved pyridine nucleotides.
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Following the onset of ischemia/reperfusion (I/R), CD38 activation occurs and is associated with depletion of NAD(P)(H) in the heart as well as myocardial injury and endothelial dysfunction. Studies with pharmacological inhibitors suggest that the NADP+-hydrolyzing ability of CD38 can deplete the
Antithrombotic therapy and the transition to the catheterization laboratory in UA/NSTEMI.
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The management of unstable angina/non ST elevation myocardial infarction (UA/NSTEMI) has evolved substantially in recent years. Multiple new antithrombotic options are available; in addition, the use of interventional strategies in patients with UA/NSTEMI has become the dominant strategy,
Discovery of Novel Small Molecule Inducers of Heme Oxygenase-1 that Protect Human iPSC-derived Cardiomyocytes from Oxidative Stress.
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Oxidative injury to cardiomyocytes plays a critical role in cardiac pathogenesis following myocardial infarction. Transplantation of stem cell-derived cardiomyocytes has recently progressed as a novel treatment to repair damaged cardiac tissue but its efficacy has been limited by poor survival of
[Inhibition of platelet aggregation for the secondary prevention after ACS: when clopidogrel instead of ASA, when clopidogrel and ASA?].
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Long-term inhibition of platelet aggregation is essential for the secondary prevention after acute coronary syndromes (ACS). Inhibition of platelet aggregation with acetylsalicylic acid (ASA) has been established as a safe and effective therapy in this indication already end of the eighties in the
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