Trials in white rats have shown, that intravenous injection of pituitrin (10 U/kg), challenging marked pulmonary edema, resulted in decrease of general lipids in them, as well as cholesterol, phospholipids and free fatty acids with accumulation of lipid peroxidation (LP) products. Preliminary administration of antioxidant emoxipin prevented the decrease in the level of general lipids, phospholipids and fatty acids, promoted a further decrease in cholesterol concentration in them and strongly inhibited lipid peroxidation processes. All this was combined with the development of more pronounced pulmonary edema. Intratracheal administration of a strong inductor of LP--Butyl hydroperoxide has never resulted in the development of pulmonary edema in white rats. These and earlier obtained data ground the statement, that LP--products are not pathogenic in the development of pulmonary edema. Inhibition of their formation may increase its development due to intensification of the signal from the receptor towards intracellular effector systems.