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Abstract
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. A simultaneous increase in the content of membrane phosphatidylserine is the mechanism of activation of opioid receptors, which plays a compensatory role.
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