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Lysophosphoglycerides including lysophosphatidyl choline (LPC), accumulate in ischemic myocardium, and in comparable concentrations induce electrophysiological alterations in vitro analogous to those seen in ischemic myocardium in vivo. The present study was performed to assess the amount of 14C-LPC incorporated into isolated tissue required to induce electrophysiological effects, to localize the sites of incorporation by electron microscopic autoradiography, and to assess the association between electrophysiological recovery and metabolism of incorporated LPC. “C-LPC (200 /J.M)” induced marked electrophysiological effects in Purkinje fibers when only 2.3% of cellular phospholipid was supplanted by exogenous LPC. Electrophysiological depression correlated with incorporation of LPC, and electrophysiological recovery correlated with metabolism of LPC to free fatty acid and phosphatidyl choline. Incubation of ventricular muscle strips with 14C-LPC (100;UM) resulted in incorporation of 0.42 nmol/mg protein of exogenous LPC at pH 7.4. Incorporation was similar at pH = 6.7 (0.36 nmol/mg protein), although electrophysiological derangements were markedly enhanced. Electron microscopic autoradiography showed that incorporated LPC was localized primarily to the sarcolemmal membrane. These findings indicate that incorporation of as little LPC as 1% of cellular phospholipid induces marked electrophysiological changes, that LPC rather than its major metabolites, fatty acid and phosphatidyl choline, are responsible for the electrophysiological alterations, and that reduction in pH enhances the membrane effects of LPC without increasing incorporation.

circulation research

Incorporation of radiolabeled lysophosphatidyl choline into canine Purkinje fibers and ventricular muscle. Electrophysiological, biochemical, and autoradiographic correlations.