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Multilamellar phosphatidylcholine liposomes have been shown to possess antibacterial activity with respect to Pseudomonas aeruginosa and Staphylococcus aureus. An increase in the level of lipid peroxidation products in liposomal suspension as the consequence of the earlier oxidation of liposomal lipid leads to a considerable increase in the antibacterial activity of liposomes. The pH of the liposomal suspension has also an essential influence on its activity. If the pH of the suspension has acidic values, its antibacterial activity increases. The bactericidal action of liposomal suspension is more pronounced with respect to S. aureus, than to P. aeruginosa.

In 30 experiments on mongrel dog hearts it was shown that 30 min of total ischemia (37 degrees C) followed by accumulation of MDA in the SR membranes and decrease of their Ca2+-uptake, but had no effect on activity Ca2+-ATPase. After 60-120 min ischemia marked a decrease of Ca2+-uptake and activity Ca2+-ATPase took place, MDA content remained at the increased level. The results show that lipid peroxidation take part in the increase of the permeability of SR membranes for Ca2+ and inhibiting of Ca2+-ATPase.

Effects of oxidized yolk phospholipids (PL) on the coronary perfusion rate (CPR) and myocardial contractility were studied in the experiments with the isolated or isolated and 30-minute ischemia-induced heart of the rat or isolated myocardial strip of the frog. The oxidized PL were demonstrated to possess a more pronounced and steady negative inotropic effect than unoxidized PL, which was due to their direct dose-dependent damaging action on myocardial contractility. The oxidized PL also made the unrestored CPR worse in the early postischemic period, the concomitant administration of aspirin producing no effects and that of the antioxidant ionol making ischemic myocardial contractility better. The findings suggest that the circulating oxidized PL may contribute to the impairment of coronary tone and contractility of the intact or ischemic myocardium and the induction of endogenous processes of lipid peroxidation plays a role in showing these effects.