Membrane phospholipids and plasmalogens in the ischemic myocardium.

This review begins with discussion concerning the effects of changes in phospholipid compositions on membrane functions. Next, pathogenetic mechanisms of ischemic cell damage are reviewed; a) membrane phospholipid breakdown, caused by the activation of phospholipases, as well as the intracellular Ca2+ overload, and b) univalent oxygen reduction and lipid peroxidation, probably all play important roles. Consequently, hydrophilic metabolites of lipid peroxidation may accumulate in the hydrophobic membrane bilayer during ischemia, causing membrane dysfunction. Free radicals may involve the cross-linking of membrane proteins as well. Previous results in support of the free radical hypothesis of myocardial ischemic injury are described; they were obtained from ESR studies, measurements of tissue antioxidants, determinations of lipid breakdown products, and studies using scavengers. The distribution, biosynthesis and physical-chemistry of plasmalogens are then discussed. Excepting the platelet activating factor recently discovered, only fragmentary information is available concerning the function of plasmalogens. It is possible that membrane plasmalogens, which contain large amounts of polyunsaturated fatty acids, are vulnerable to free radical/ischemic injury.