EVIDENCE OF A TEMPERATURE-SENSITIVE STEP IN THE RELEASE OF PROSTAGLANDIN E(2) IN CALCIUM IONOPHORE-STIMULATED RAT MUSCLE

Recent studies have shown that mild hypothermia (32-35 degrees C) conf ers striking protection against ischemic muscle and neuronal injuries, although the mechanisms are unknown, We previously demonstrated that the release of prostaglandin E(2) (PGE(2)) from metabolically stressed muscles was dependent on calcium and was abolished at or below 35 deg rees C. In this study, we examined the temperature response of the rel ease of arachidonic acid (AA) and its cyclooxygenase metabolites, PGE( 2) and prostaglandin F-2 alpha (PGF(2 alpha)) from rat skeletal muscle in the presence of calcium ionophore A23187, an agent that directly e levates intracellular calcium. Calcium ionophore markedly stimulated t he release of AA, PGE(2) and PGF(2 alpha) at 37 degrees C, as expected , Reducing the temperature to 35 degrees C and below sharply decreased PGE(2) and PGF(2 alpha) release but not AA release, The activity of p hospholipase A(2) stimulated by calcium ionophore was unaffected when temperature of incubation was lowered from 37 to 32 degrees C, The res ults suggest that reducing temperature from 37 degrees C to 35 degrees C or below inhibits the conversion from free arachidonate to PGs in c alcium ionophore-stimulated muscle.