In isolated ischemic rat hearts, the presence of palmitate as a metabolic substrate exacerbates morphological damage and mechanical dysfunction compared to glucose alone.
May worsen ischemic injury in animal models; leaves open whether fatty acid restriction improves human outcomes.
The ultrastructure, function, and metabolism of isolated rat hearts perfused under control or ischemic conditions were investigated. Either both glucose (11 mM) or glucose and palmitic acid (1.5 mM) were used as metabolic substrates. A 60-min period of whole-heart ischemia, i.e., a 60% initial reduction in coronary flow, resulted in a more dramatic morphological alteration in those hearts receiving palmitate compared to those receiving glucose as the only substrate. In ischemic hearts receiving palmitate, intramitochondrial osmiophilic amorphous densities of both rounded and elongated types were observed. These amorphous densities did not develop in ischemic hearts receiving glucose alone over the same period of ischemia. Such morphological alterations were associated with a more severe deterioration of mechanical function in the presence of palmitate. Both ischemic conditions resulted in increased tissue levels of acyl esters of CoA and carnitine, but the rise in levels of long-chain acyl carnitine was about two times greater in those ischemic hearts receiving palmitate.
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D. Feuvray (1981) studied this question.
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