Hagve T A, Sprecher H, Hohl C M
Department of Physiological Chemistry, College of Medicine, Ohio State University, Columbus 43210.
J Mol Cell Cardiol. 1990 Dec;22(12):1467-75. doi: 10.1016/0022-2828(90)90989-f.
In ischemic myocardium abnormal lipid metabolism results in accumulation of compounds that are deleterious to membrane structural integrity and membrane dependent functions. In this study isolated adult rat ventricular myocytes were used to investigate anoxia-induced alterations in cellular lipid composition and metabolism. Myocyte phospholipid content declined 19% on average during 60 min anoxia and intracellular arachidonic acid increased 3-fold, without affecting myocyte ATP content. Anaerobic incubation in the absence of glucose depleted cellular ATP to 2 nmol/mg protein, elicited a 23% decrease in phospholipids, and reduced triacylglycerol content by 51%. Intracellular levels of C16-C22 fatty acids were significantly elevated, especially palmitic and arachidonic acids. Myocytes presented with 0.08 mM [1-14C]-palmitic or arachidonic acid acylated 85% (25-26 nmol/mg) of the fatty acid taken up into triacylglycerols. Anoxia decreased this esterification by 46-60%. Formation of [14C]-CO2 was also depressed 70-90% by anaerobiosis. The results demonstrate that anoxia stimulates degradation of complex lipids, with a concomitant increase in non-esterified fatty acids, especially arachidonic acid.
