BRAIN ADAPTATION TO CHRONIC HYPOBARIC HYPOXIA IN RATS
BRAIN ADAPTATION TO CHRONIC HYPOBARIC HYPOXIA IN RATS
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DOI：
10.1152/jappl.1992.72.6.2238
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发表时间：
1992-06-01
影响因子：
3.3
通讯作者：
FARRELL, RM
中科院分区：
文献类型：
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作者：
LAMANNA, JC;VENDEL, LM;FARRELL, RM
大鼠暴露于低压缺氧（0.5大气压）长达3周。低血糖大鼠体重没有增加，但保持正常的脑水和离子含量。与同窝对照组相比，缺氧3周后血液红细胞压积增加48%至71%。暴露于10%常压氧15分钟的大鼠脑血流量平均增加38%，3小时后增加23%，但缺氧3周后与常压常氧大鼠无差异。在任何低氧条件下，作为脑血浆体积的量度的蔗糖空间都没有改变。平均脑微血管密度在额极大脑皮层增加76%，在额叶运动皮层增加46%，在额叶感觉皮层增加54%，在顶叶运动皮层增加65%，在顶叶感觉皮层增加68%，在海马CA1区增加68%，在海马CA3区增加57%，在纹状体增加26%，在小脑增加56%。结果表明，缺氧引起三种主要的影响脑氧利用率的反应。缺氧的急性效应是局部血流量增加，在持续缺氧暴露时恢复到对照水平。持续中度低氧暴露的长期影响是红细胞生成和血管生成导致的毛细血管间距减少。血细胞比容的升高和微血管密度的增加共同增加了大脑的氧可用性，使其在正常范围内，尽管这并不意味着组织PO2恢复正常。
Rats were exposed to hypobaric hypoxia (0.5 atm) for up to 3 wk. Hypoxic rats failed to gain weight but maintained normal brain water and ion content. Blood hematocrit was increased by 48% to a level of 71% after 3 wk of hypoxia compared with littermate controls. Brain blood flow was increased by an average of 38% in rats exposed to 15 min of 10% normobaric oxygen and by 23% after 3 h but was not different from normobaric normoxic rats after 3 wk of hypoxia. Sucrose space, as a measure of brain plasma volume, was not changed under any hypoxic conditions. The mean brain microvessel density was increased by 76% in the frontopolar cerebral cortex, 46% in the frontal motor cortex, 54% in the frontal sensory cortex, 65% in the parietal motor cortex, 68% in the parietal sensory cortex, 68% in the hippocampal CA1 region, 57% in the hippocampal CA3 region, 26% in the striatum, and 56% in the cerebellum. The results indicate that hypoxia elicits three main responses that affect brain oxygen availability. The acute effect of hypoxia is an increase in regional blood flow, which returns to control levels on continued hypoxic exposure. Longer-term effects of continued moderate hypoxic exposure are erythropoiesis and a decrease in intercapillary distance as a result of angiogenesis. The rise in hematocrit and the increase in microvessel density together increase oxygen availability to the brain to within normal limits, although this does not imply that tissue PO2 is restored to normal.