Effect of Endotoxin and Platelet-activating Factor on Lipid Oxidation in the Rat Heart

The effects of endotoxin and platelet-activating factor (PAF) administeredin vivoandin vitroon lipid oxidation by isolated perfused working rat heart were investigated and compared. Endotoxin administeredin vivodecreased oleate oxidation in perfused hearts and caused increased accumulation of lipid in myocardial tissue; this was accompanied by a dose-dependent inhibition of cardiac mechanical function. There was no effect on triolein (chylomicron) oxidation. By contrast, PAF administeredin vivocaused a small (non-significant) increase in the oxidation rate of oleate and triolein, and also increased myocardial lipoprotein lipase activity. Cardiac mechanical function was not inhibited by PAF—indeed pretreatment of animals by PAF administeredin vivoprotected the heart from the decline in function associated with subsequent fatty acid perfusion. Administration of endotoxin during perfusionin vitrodid not affect oleate or triolein oxidation and cardiac mechanical function was unchanged; PAF administeredin vitrocaused an early increase in oleate oxidation and a later increase in triolein oxidation. Administration of both endotoxin and PAFin vitroincreased myocardial lipoprotein lipase activity. PAF is unlikely to be responsible for all of the effects of endotoxin on cardiac lipid metabolism.