Ischemia-induced inhibition of active calcium transport into gerbil brain microsomes: Effect of anesthetics and models of ischemia

The excessive increase in intracellular Ca2+ concentration is associated wi th events linking cerebral blood flow reduction to neuronal cell damage. We have investigated the possible effect of ischemia and ischemia-reperfusion injury on endoplasmic reticulum (ER) Ca2+ transport. Two different models of ischemia as well as two different anesthetics were used. 5 min and 15 mi n of global forebrain ischemia caused significant depression of the rate of microsomal Ca2+ accumulation in pentobarbital anesthetised gerbils. The Ca 2+ uptake activity recovered partially after 1 hour of reperfusion. Unlike pentobarbital anesthetised gerbils, no significant changes were detected in the active microsomal Ca2+-transport after 10 min of global forebrain isch emia in gerbil forebrain and hippocampus under halothane anesthesia. In add ition, using the model of decapitation ischemia, we observed significant ch anges of the Ca2+ uptake in both halothane and pentobarbital anesthetised g erbils. These findings indicate that ischemic insult alters the brain micro somal Ca2+ transport which is not due to inhibition of the Ca2+-ATPase acti vity. However, the effect of ischemia on this transport system is dependent on the model of ischemia and on the type of anesthetics.