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pepstatin/infarction
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Role of cellular proteinases in acute myocardial infarction. I. Proteolysis in nonischemic and ischemic rat myocardium and the effects of antipain, leupeptin, pepstatin and chymostatin administered in vivo.
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To test the hypothesis that cellular proteinases contribute to ischemic myocellular death, measurements were made of tyrosine release (an index of overall proteolysis) from incubated slices of nonischemic and ischemic myocardium obtained at various times after coronary artery occlusion in rats.
Role of cellular proteinases in acute myocardial infarction. II. Influence of in vivo suppression of myocardial proteolysis by antipain, leupeptin and pepstatin on myocardial infarct size in the rat.
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Cultured myofibroblasts generate angiotensin peptides de novo.
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Scar tissue found at the site of myocardial infarction (MI) contains phenotypically transformed fibroblast-like cells termed myofibroblasts (myoFb). In injured cardiac tissue, autoradiography and immunolabeling have localized high density angiotensin (Ang) converting enzyme (ACE) and Ang II receptor
Mechanism of interference by haemolysis in the cardiac troponin T immunoassay.
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BACKGROUND
The cardiac troponins have been shown to be sensitive and specific biochemical markers of myocardial infarction and highly prognostic for future adverse events in patients with acute coronary syndromes. There have been reports suggesting that haemolysis causes a negative interference in
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