Post-ischemic coma in rat: effect of different pre-ischemic blood glucose levels on cerebral metabolic recovery after ischemia.
Post-ischemic coma in rat: effect of different pre-ischemic blood glucose levels on cerebral metabolic recovery after ischemia.
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大鼠缺血后昏迷：不同缺血前血糖水平对缺血后脑代谢恢复的影响。
DOI：
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发表时间：
1980
期刊：
影响因子：
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通讯作者：
Albert Gjedde
中科院分区：
文献类型：
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作者：
E. Siemkowicz;Albert Gjedde
将高血糖、正常血糖和低血糖大鼠暴露于10分钟的完全脑缺血。在缺血前、缺血后3分钟和60分钟分别测定局部脑血流量（CBF）、血脑葡萄糖转运、脑氧和葡萄糖消耗。缺血后3 min，3组大鼠之间没有观察到差异。缺血后1小时，高血糖大鼠与其他组相比，具有相似的全脑CBF和葡萄糖消耗，但明显较低的耗氧量，表明高血糖组中葡萄糖的持续非氧化使用。在一般情况下，局部CBF值超过对照值的100-200%，缺血后3分钟，缺血后1小时，大鼠仍处于昏迷状态，减少到对照的50%。然而，在高血糖大鼠的脑干中，血流量在缺血后仍然升高。因此，在缺血前、缺血中和缺血后观察到的高血糖大鼠死亡率显著增加（Siemkowicz &汉森1978）不是缺血后CBF受损的结果，而是脑细胞缺血或缺血后损伤的结果。我们认为高血糖组的损害因素是与长时间无氧糖酵解相关的乳酸中毒增加。
Hyper-, normo-, and hypoglycemic rats were exposed to 10 min of complete cerebral ischemia. Regional cerebral blood flow (CBF), blood-brain glucose transfer, and cerebral consumption of oxygen and glucose were measured before, as well as three and 60 minutes after ischemia. Three min after ischemia, no differences were observed between the 3 groups of rats. One h after ischemia, the hyperglycemic rats in comparison to those of the other groups had similar whole-brain CBF and glucose consumption but appreciately lower oxygen consumption, indicating continued non-oxidative use of glucose in the hyperglycemic group. In general, regional CBF values exceeded the control value by 100-200% 3 min after ischemia and were reduced to 50% of control at 1 h after ischemia, at which time the rats were still comatose. In the brain stem of hyperglycemic rats, blood flow, however, remained elevated after ischemia. Thus, the significantly increased mortality observed in rats hyperglycemic before, during and after ischemia (Siemkowicz & Hansen 1978) was the result, not of impaired postischemic CBF, but of ischemic or postischemic damage to brain cells. We suggest that the damaging factor in the hyperglycemic group is increased lactacidosis associated with prolonged anaerobic glycolysis.