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pyridine/infarction

הקישור נשמר בלוח
מאמריםניסויים קלינייםפטנטים
עמוד 1 מ 32 תוצאות

Effects of energostim on the sympathoadrenal system and contents of pyridine nucleotides during acute myocardial infarction.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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] (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].

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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
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
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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?].

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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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