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Kléber AG. Consequences of acute ischemia for the electrical and mechanical function of the ventricular myocardium. A brief review. Experientia. 1990;46(11):1162-7doi: 10.1007/BF01936928.
Kléber, A. G. (1990). Consequences of acute ischemia for the electrical and mechanical function of the ventricular myocardium. A brief review. Experientia, 46(11), 1162-7. https://doi.org/10.1007/BF01936928
Kléber, A G. "Consequences of acute ischemia for the electrical and mechanical function of the ventricular myocardium. A brief review." Experientia vol. 46,11 (1990): 1162-7. doi: https://doi.org/10.1007/BF01936928
Kléber AG. Consequences of acute ischemia for the electrical and mechanical function of the ventricular myocardium. A brief review. Experientia. 1990 Dec 01;46(11):1162-7. doi: 10.1007/BF01936928. PMID: 2253715.
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Experientia. 1990 Dec 01;46(11):1162-7. doi: 10.1007/BF01936928.

Consequences of acute ischemia for the electrical and mechanical function of the ventricular myocardium. A brief review.

Experientia

A G Kléber

Affiliations

  1. Department of Physiology, University of Bern, Switzerland.

PMID: 2253715 DOI: 10.1007/BF01936928

Abstract

Reduction or interruption of the blood supply to the myocardium leads to marked disturbances of electrical and mechanical function within a few seconds. Electrical dysfunction is characterized by an initial depolarization of the resting membrane, and a decrease of the amplitude, the upstroke velocity and the duration of the action potential. Both depolarization and depression of the action potential are closely associated with intracellular metabolic acidosis. After this initial phase, electrical cell-to-cell uncoupling develops, probably as a consequence of increased cytosolic free [Ca++]. Mechanical dysfunction is characterized by a dissociation of the initial decrease of active force development from the subsequent ischemic contracture. Active force development in acute ischemia is inhibited by the accumulation of ischemic metabolic products (H+, inorganic phosphate (Pi), Mg++) but not by a marked decrease of [ATP]. The subsequent ischemic contracture is probably initiated by release of Ca++ from intracellular stores. This release causes rapid consumption of ATP and the development of rigor within 1-2 minutes.

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