Accumulation of arachidonic acid in ischemic/reperfused cardiac tissue: possible causes and consequences

摘要: Under physiological conditions, the content of unesterified arachidonic acid in cardiac tissue is very low. The bulk present membrane phospholipid pool. Incorporation into phospholipids (reacylation) and liberation this fatty from pool (deacylation) are controlled by a set finely tuned enzymes, including lysophospholipid acyltransferase phospholipase A2. At present, at least three subtypes A2 have been identified structure, i.e., low molecular mass group II A2, cytoplasmic high plasmalogen-specific A2. Cessation flow to heart (ischemia) gives rise net degradation accompanied accumulation acids, (unesterified) acid. Restoration previously ischemic cells reslts continued acids. mechanism(s) underlying ischemic/reperfused myocardial (are) incompletely understood. Impaired reacylation, enhanced hydrolysis phospholipids, or combination both may be responsible for phenomena observed. Elevated levels exert direct indirect effects on affected myocardium healthy adjacent injured cardiomyocytes. Indirect might evoked metabolites, eicosanoids. Arachidonic directly influence ion channel activity, substrate metabolism signal transduction, thereby affecting functional characteristics myocardium.