منابع مشابه
Haemostatic function in myocardial infarction.
Coagulation factor VIII, von Willebrand factor, antithrombin, fibrinogen, plasminogen activator capacity, and inhibitors of fibrinolysis, including a recently discovered fast inhibitor of tissue plasminogen activator, were measured three to six months after myocardial infarction in 116 male and 32 female patients aged less than 45 and in 136 age and sex matched random controls. Plasma concentra...
متن کاملEnzymatic and Immunogenic Changes of Myocardial Infarction
Diagnosis of myocardial infarction is very important in a patient with chest pain. Chest pain is not always present or it may be from other causes rather than myocardial infarction. Q wave is present in 30] of infarction. ST,T wave changes are present in all myocardial infarctions, but these changes also are present in myocardial ischernia. For these reasons diagnosis of myocardial infarction...
متن کاملEffect of exercise training and L-arginine supplementation on oxidative stress and left ventricular function in rats with myocardial infarction
Introduction: The aim of the present study was to evaluate the effect of exercise training and L-arginine supplementation on oxidative stress and systolic ventricular function in rats with myocardial infarction (MI). Methods: Four weeks after the surgically-induced MI, 40 male Wistar rats were randomly assigned to the following 4 groups (n=10): MI-sedentary control (Sed) MI-exercise (Ex) MI-...
متن کامل[Changes in myocardial function and perfusion after acute myocardial infarction].
Rev Esp Cardiol 2003;56(5):433-5 433 Ligation of a coronary artery causes myocardial necrosis. It has been shown in experimental animals1 that the size of the necrotic scar is directly proportional to the time elapsed between ligation and reperfusion. Early reperfusion not only reduces the size of the infarct, but also protects against ventricular dilatation. Although delayed reperfusion is una...
متن کاملCalpain inhibition preserves myocardial structure and function following myocardial infarction.
Cardiac pathology, such as myocardial infarction (MI), activates intracellular proteases that often trigger programmed cell death and contribute to maladaptive changes in myocardial structure and function. To test whether inhibition of calpain, a Ca(2+)-dependent cysteine protease, would prevent these changes, we used a mouse MI model. Calpeptin, an aldehydic inhibitor of calpain, was intraveno...
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ژورنال
عنوان ژورنال: Journal of the American College of Cardiology
سال: 1991
ISSN: 0735-1097
DOI: 10.1016/0735-1097(91)92180-t