Brain mitochondrial function after ischemia and hypoxia. I. Ischemia induced by increased intracranial pressure.
Brain mitochondrial function after ischemia and hypoxia. I. Ischemia induced by increased intracranial pressure.
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缺血缺氧后脑线粒体功能。
DOI：
10.1001/archneur.1973.00490300070009
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发表时间：
1973
期刊：
影响因子：
29
通讯作者：
T. Langfitt
中科院分区：
文献类型：
--
作者：
H. Schutz;P. R. Silverstein;M. Vapalahti;D. Bruce;L. Mela;T. Langfitt
在61只家兔上观察了“压迫性缺血”对脑线粒体活性的影响。结果表明：（1）由于状态3呼吸减少，状态4呼吸增加，呼吸控制率仅在压迫性缺血30和40分钟后才显著降低，（2）仅在压迫性缺血40分钟后才出现呼吸严重解偶联;（3）缺血40分钟后，解偶联物激活的腺苷三磷酸酶（ATP酶）仍无明显变化，但ATP酶自发活性明显升高;（4）只要维持脑灌注压，即使恢复期出现严重的高碳酸血症和低碳酸血症，也不会出现循环恢复后线粒体功能的继发性恶化。研究结果表明，在短暂的全脑缺血后，细胞成分而不是线粒体的改变是造成不可逆脑损伤的原因。
The effect of "compression ischemia" on brain mitochondrial activity was examined in 61 rabbits. We found that (1) the respiratory control ratio was significantly decreased only after 30 and 40 minutes of compression ischemia due to a decrease in state 3 and an increase in state 4 respiration; (2) heavy uncoupling of respiration occurred only after 40 minutes of compression ischemia; (3) uncoupler-activated adenosine triphosphatase (ATPase) was not impaired even after 40 minutes of ischemia, but spontaneous ATPase activity increased significantly; (4) secondary deterioration of mitochondrial function after circulatory recovery did not occur even with severe hypercapnia and hypocapnia in the recovery period as long as the cerebral perfusion pressure was maintained. The findings suggest that alterations in constituents of the cell other than the mitochondria are responsible for irreversible brain damage following brief periods of total cerebral ischemia.