Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
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Research Abstract |
Although previous clinical reports suggested the prophylactic effects of hypothermia and/or general anesthetics against cerebral ischemia, the cellular mechanisms by which hypothermia and/or anesthetics protect brain tissue against hypoxia remain unknown. In the present study, we have employed the rat hippocampal slice preparations in vitro, and studied the effects of hypothermia and general anesthetics against anoxia using electrophysiological techniques. Extracellular recordings were used to record field potentials in CA1 pyramidal neurons of rat hippocampal slices. Slices were placed on a liquid/gas interface, and were perfused with 95%O_2/5%CO_2 and artificial cerebrospinal fluid (37℃). Anoxia (0% oxygen) was applied to slices by switching the gas mixture from 95%O_2/5%CO_2 to 95%N_2/5%CO_2 in the absence and presence of hypothermia (27℃) and/or general anesthetics (thiopental, propofol, volatile anesthetics). The 180-sec anoxia induced anoxic depolarization (AD) in hippocampal slices at 37℃ in the absence of general anesthetics. Since combination of the NMDA, non-NMDA, and GABA receptor antagonists failed to prevent AD, synaptic transmission is not responsible for elicitation of AD. The treatment with thiopental, but not propofol and volatile anesthetics, significantly reduced the incidence of AD. The hypothermia alone reduced the incidence of AD, and accelerated the reduction in the presence of thiopental. The present study clearly demonstrated that the treatment with hypothermia and/or thiopental prevent AD, and produce prophylactic actions against ischemia in hippocampal slice preparations in vitro.
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