ABSTRACT
Lack of oxygen has profound effects on myocardial lipid homeostasis. This chapter attempts to describe the effect of ischemia and reperfusion on myocardial fatty acid metabolism in relation to reversible and irreversible injury of myocardial tissue. The mechanism underlying impairment of myocardial phosphoglyceride homeostasis during ischemia and reperfusion is incompletely understood. Enhanced degradation and/or reduced resynthesis have to be considered. In addition, labilization of myocardial membranes by the action of oxygen free radicals, making the phosphoglyceride molecules more prone to endogenous phospholipase activity, might offer a feasible explanation for the recent observations. When the ischemic period prolongs, nonesterified fatty acids (NEFA) start to accumulate in the tissue affected. The substantial contribution of arachidonic acid to the NEFA accumulated indicates the persistance of impaired phosphoglyceride metabolism in the reperfused tissue. Reinstallation of flow through the previously ischemic tissue results in an enhanced accumulation of NEFA, including arachidonic acid.
