Jan 1, 1976

Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion

Acta Medica Scandinavica. Supplementum
P R Maroko, E Braunwald

Abstract

A number of hemodynamic, pharmacologic and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, external counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (elevation of coronary perfusion pressure by alpha-adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (mannitol, hypertonic glucose); presumably by augmenting anaerobic metabolism (glucose-insulin-potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen r...Continue Reading

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Mentioned in this Paper

Metabolic Process, Cellular
Glucagon (rDNA)
Necrosis
Plasma Osmolality Measurement
Oxygen Measurement, Partial Pressure, Arterial
Ouabain
Myocardium
Autolysis
Coronary Occlusion
Digitalis preparation

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