Lysophosphatidylcholine and sodium-calcium exchange in cardiac sarcolemma: comparison with ischemia

Abstract

Lysophosphoglyceride accumulation in ischemic myocardium has been hypothesized to be a mechanism for altered sarcolemmal properties that underlie electrophysiological changes and Ca2+ accumulation in ischemia. We find that in vitro application of lysophosphatidylcholine to normal canine sarcolemmal vesicles at a concentration of 0.3 mumol/mg sarcolemmal protein inhibits Na(+)-Ca2+ exchange. Both maximum velocity (Vmax) for Ca2+ transport and Ca2+ affinity are reduced by lysophosphatidylcholine, whereas in ischemia only Vmax is reduced [M. M. Bersohn, K. D. Philipson, and J. Y. Fukushima. Am. J. Physiol. 242 (Cell Physiol. 11): C288-C295, 1982]. This amount of lysophosphatidylcholine does not affect sarcolemmal passive permeability to either Ca2+ or Na+. Treatment of sarcolemma with phospholipase A2 sufficient to inhibit Na(+)-Ca2+ exchange velocity by 50% causes large increases in sarcolemmal lysophosphatidylcholine and lysophosphatidylethanolamine. On the other hand, 1 h of ischemia in rabbit hearts does not affect sarcolemmal phospholipid composition. Thus, although in vitro treatment with lysophosphatidylcholine or phospholipase A2 has profound effects on sarcolemmal properties, sarcolemmal accumulation of lysophosphatidylcholine cannot account for the effects of ischemia as measured in highly purified sarcolemmal vesicles from ischemic hearts.