[Effects of @entity592 on histological and behavioral outcome in @entity35 @entity1249 hippocampus after global transient XXXX ].

@entity4485 @entity2227 @entity2806 @entity63 @entity1249 @entity1508 @entity575 @entity143 @entity460 @entity35 @entity1604 @entity592 @entity10457 @entity528
Evidence suggests that @entity528 may ultimately be the result of excessive intracellular @entity460 accumulation. In principle, abnormal @entity460 concentrations during @entity63 are derived from three main sources: exaggerated influx via (a) voltage-operated channels, (b) receptor-controlled channels (f. ex. @entity143 ) and (c) the release of intracellular @entity460 ion stores. Previous studies using either @entity460 channel blockers or @entity143 antagonists have demonstrated only limited protective effects of these agents in global transient @entity2806 , whereas little or no attention has been paid to the @entity460 sources listed under (c). @entity592 has been shown to block the increase in free intracellular @entity460 ion stimulated by either @entity143 or @entity2227 . Thus we postulated that @entity592 might improve neuronal survival in vulnerable regions to @entity63 such as the @entity1249 hippocampus. Male @entity35 (300 approximately 400 g) were prepared for a four-vessel occlusion model of @entity2806 . @entity2806 was induced by snaring the carotid arteries for 15 mins and maintaining mean arterial pressure at 80 mmHg. Strict attention was paid to keep normal blood gas values. Following @entity63 @entity1508 anesthesia was discontinued, and @entity35 were extubated and when stable transferred to cages with free access to water and food. @entity35 survived for 7 days under close supervision, after which they were anesthetized with @entity4485 and perfused transcardially with 4% @entity1604 / @entity10457 buffer. The brain was removed and placed in fresh fixatives for another 7 days, after which 40 microns sections were cut and @entity575 -stained.(ABSTRACT TRUNCATED AT 250 WORDS)
