虚血性脳浮腫に対するCa拮抗剤(nicardipine hydrochloride)の効果
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The author tested the effect of the Ca-antagonist nicardipine hydrochloride on the development of post-ischemic cerebral edema. Global ischemia lasting for 30 minutes was experimentally produced in rats by means of Pulsinelli's technique, following which brain circulation was reinstituted. The animals were divided into three groups. The rats in Group 1 received a single intravenous injection of 0.05 mg/kg of nicardipine prior to the onset of ischemia. Group 2 were given the same pretreatment as those in Group 1 and also received daily intraperitoneal injections of 0.1 mg/kg of nicardipine for 7 days after the ischemic insult. Group 3 comprised untreated control animals. The changes in water content, free fatty acids, and extracellular concentrations of K^+ and Ca^<++> ions in the brain during and after ischemia were measured by means of a gravimeter, gas chromatography, and double ion-sensitive microelectrodes, respectively. Survival rates in Group 1 (54.5%) and Group 2 (84.6%) at 7 days after recirculation were significantly higher than that in the control group (23.1%). Significant increases in the cerebral water content of the controls were observed at two peaks, the first at 30 minutes (early edema) and the second at 72 hours (late edema) following recirculation. Late edema did not develop in the Group 2 animals. In control rats, the brain free fatty acid concentration increased 4-fold during ischemia and rapidly normalized shortly after recirculation. The accumulation of free fatty acids was thought to reflect an ischemia-induced increase in Ca-dependent catabolism. However, premedication with nicardipine did not modify the change in the free fatty acid concentration during or after ischemia. Electrophysiological study of the cerebral cortex during ischemia revealed an increase in extracellular K^+ ions followed by a decrease in extracellular Ca^<++> ions, suggesting that there was an influx of Ca into intracellular compartments. This Ca influx was suppressed in 43.5% of the animals treated with nicardipine. Nicardipine appears to suppress the development of late cerebral edema during recirculation following a 30-minute global ischemic insult in rats. However, the data indicate that this suppression is not directly related to the effect of nicardipine on free fatty acid metabolism.
- 社団法人 日本脳神経外科学会の論文
- 1987-09-15