Degradation of Membrane Phospholipids in the Ischemic and Reperfused Heart

Abstract

Under normal circumstances cardiac cells provide sufficient amounts of energy by oxidative degradation of substrates such as fatty acids, glucose and lactate to fulfil their energy requirements. Contraction and relaxation of the myofibrils consume over 70 of ATP produced by mitochondrial activity, the remaining part is used for transport of ions across membranes, and maintenance of cellular integrity. The plasmalemma, the membrane enclosing the content of living cells, plays a crucial role in the complex process of maintenance of integrity. As soon as the plasmalemma is no longer capable of maintaining a barrier between the extracellular and intracellular compartments, the cell will die (1). Loss of semi-permeable properties of the plasmalemma results in release of metabolites and cytoplasmic proteins, required for enzymatic or transport processes, and influx of extracellular macromolecules and calcium ions into the interior of the injured cell (1). This condition, usually designated as cell death, will be followed by degenerative changes such as lysis of the cellular remnants by lysosomal enzymes and by macrofages invading the damaged area of the heart. A variety of pathophysiological derangements may lead to death of cardiac cells. The most common cause of cellular injury and cell death is ischemia (insufficient blood supply to the heart). Restoration of flow to previously ischemic areas may inflict additional damage upon the injured cells.