PMID: 9173719Jan 1, 1997Paper

Cellular sequelae of myocardial ischemia

Zeitschrift für Kardiologie
G Richardt, R Tölg

Abstract

The interruption of arterial oxygen delivery to the myocardium during myocardial ischemia leads to a breakdown in oxidative phosphorylation and to a temporary formation of energy-rich phosphates by anaerobic glycolysis. However, the accumulation of the produced metabolites NADH, lactate and H+ rapidly blocks the key enzymes of glycolysis, so that a sufficient content of ATP necessary for cellular functions can no longer be maintained. Further accumulation of metabolic endproducts induces direct cellular damage by mitochondrial swelling and Ca2+ overload. The early contractile dysfunction can be attributed to a diminished intracellular Ca2+ release and to cellular acidosis. Furthermore, the cellular loss of K+ and anions influences the electrophysiological integrity, while the myocytic Ca2+ overload activates cellular proteases and lipases and blocks mitochondrial phosphorylation. In the later ischemic period an increased noradrenaline release from the cardiac sympathetic nerves leads to an increased adrenergic activation and promotes the occurrence of malignant arrhythmias. On the other hand, myocardial ischemia is able to induce specific, protective proteins. The transition from reversible to irreversible cellular injury is no...Continue Reading

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