Effect of Phosphatidylcholine Nanosomes on Phospholipid Composition of the Plasma Membranes in Liver Cells and Blood Serum in Experimental Atherosclerosis.

Alimentary atherosclerosis is associated with a significant decrease in the content of phosphatidylcholine, the phospholipid that provides antioxidant protection, in the plasma membrane of liver cells, while the level of phosphatidic acid that initiates generation of superoxides, on the contrary, increases. The level of membrane phosphatidylserine, a target of the scavenger receptors, which initiates removal of damaged cells and modified lipoproteins from the circulation was also elevated. In the blood serum of rabbits receiving an atherogenic diet, the content of cardiolipin involved in the immune mechanisms of atherosclerosis development and a risk factor for thrombosis, sharply increased.

Phospholipid-Dependent Mechanisms of Platelet Dysfunction in Rabbits with Hemorrhagic Shock.

The time course of phospholipid composition of platelet plasma membranes at the peak of hemorrhagic shock were studied in rabbit experiments. The results indicate the key role of impairment of the structure of platelet membrane phospholipid bilayer in the pathogenesis of shockogenic thrombocytopathy.

Phospholipids in mitochondrial dysfunction during hemorrhagic shock.

Energy deficiency plays a key role in the development of irreversible shock conditions. Therefore, identifying mitochondrial functional disturbances during hemorrhagic shock should be considered a prospective direction for studying its pathogenesis. Phospholipid (PL)-dependent mechanisms of mitochondrial dysfunction in the brain (i.

Changes in phospholipid composition of cardiomyocyte plasma membranes during hemorrhagic shock.

Changes in the phospholipid composition of cardiomyocyte plasma membranes during hemorrhagic shock suggest that disturbances in phosphatidylethanolamine metabolism serve as one of the major factors for myocardial alteration in shock. Depletion of membrane phosphatidylcholine causes destruction of cardiomyocytes. The enhanced breakdown of membrane sphingomyelin at the late stage of hemorrhagic shock is considered as a mechanism, which induces apoptosis in cardiomyocytes and Ca(2+) accumulation in these cells.