Energy and Cation Control in the Reoxygenated Myocardial Cell
The development of cell injury in ischemic tissue starts with a deficit in the cellular balance of energy. The energetic deficit leads to a slowdown or cessation of important metabolic functions, among these the cellular control of Na+ and Ca 2+ ions. When the cellular reserves of energy are depleted, cation pumps regulating the normal intracellular ionic milieu fail due to a lack of energy. A lone-lasting overload of the cytosolic space and intracellular organelles with excess Car 2+ can be deleterious for the cell, as a number of structure degrading processes may become activated. In muscle cells, the activation of the myofibrillar contractile apparatus by high levels of Ca 2+ may additionally cause mechanical cell damage. The loss of cellular Ca 2+ homeostasis is a sign of advanced, but not necessarily irreversibly cell injury. For a better understanding of the pathogenesis of progressive myocardial injury the energy and cation control in the oxygen deprived and reoxygenated cardiomyocyte must be analyzed. This article provides a brief review.
KeywordsSarcoplasmic Reticulum Myocardial Cell Intracellular Acidosis Contractile Machinery Cation Control
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