The myocardial content of fatty acids and phospholipids during the calcium paradox

Abstract

Readmission of Ca2+ after a short period of Ca2+-free perfusion results in a rapid and massive release of cytoplasmic proteins from the heart (calcium paradox). Maximal release rates of proteins are already reached within 2 min after Ca2+ repletion. The precise mechanism underlying the loss of cellular membrane integrity, resulting in the loss of intracellular proteins, has not been clearly defined. The present study indicates that neither substantial degradation of phospholipids, being important constituents of myocardial membranes, nor accumulation of fatty acids occur during the early phase (within 1.5 min) of Ca2+ readmission. Thereafter significant amounts of such fatty acids as arachidonic acid accumulate in the Ca2+ repleted hearts. The late onset of arachidonic acid accumulation, most likely reflecting phospholipid degradation, is considered to be an epiphenomenon occurring in myocardial cells which became heavily damaged, as indicated by the substantial loss of lactate dehydrogenase, during the early phase of Ca2+ repletion. Interestingly, tissue fatty acid levels increased already significantly during the Ca2+-free perfusion period (by about 240%). The significance of this finding is not completely understood. A possible causal relationship with disturbed ion homeostasis during the induction of calcium paradox remains to be established.