Recent studies have shown that mild hypothermia (32-35 degrees C) confers striking protection against ischemic muscle and neuronal injuries, although the mechanisms are unknown. We previously demonstrated that the release of prostaglandin E2 (PGE2) from metabolically stressed muscles was dependent on calcium and was abolished at or below 35 degrees C. In this study, we examined the temperature response of the release of arachidonic acid (AA) and its cyclooxygenase metabolites, PGE2 and prostaglandin F2 alpha (PGF2 alpha) from rat skeletal muscle in the presence of calcium ionophore A23187, an agent that directly elevates intracellular calcium. Calcium ionophore markedly stimulated the release of AA, PGE2 and PGF2 alpha at 37 degrees C, as expected. Reducing the temperature to 35 degrees C and below sharply decreased PGE2 and PGF2 alpha release but not AA release. The activity of phospholipase A2 stimulated by calcium ionophore was unaffected when temperature of incubation was lowered from 37 to 32 degrees C. The results suggest that reducing temperature from 37 degrees C to 35 degrees C or below inhibits the conversion from free arachidonate to PGs in calcium ionophore-stimulated muscle.
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