PROLONGED ANOXIC SURVIVAL DUE TO ANOXIA PRE-EXPOSURE - BRAIN ATP LACTATE + PYRUVATE
PROLONGED ANOXIC SURVIVAL DUE TO ANOXIA PRE-EXPOSURE - BRAIN ATP LACTATE + PYRUVATE
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DOI：
10.1152/ajplegacy.1964.207.2.452
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发表时间：
1964-01-01
影响因子：
--
通讯作者：
BALFOUR, WM
中科院分区：
文献类型：
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作者：
DAHL, NA;BALFOUR, WM
接受短暂缺氧的大鼠可以在第二次缺氧中存活90秒，而对照组动物的存活时间为60秒。在第二次暴露期间，大脑中ATP浓度的较慢消失表明，这种较长的存活时间是由于大脑能量代谢的改变。预先暴露的动物的大脑初始ATP浓度并不高于对照组。当在缺氧测试前用碘乙酸酯抑制糖酵解时，暴露前的优势消失，这表明存活时间更长可能是由于增加了厌氧糖酵解。在缺氧期间，预暴露动物的大脑中乳酸积累的速度比对照组更快，这表明厌氧糖酵解增加是延长存活时间的原因。这种影响并不是由于大脑葡萄糖浓度升高所致。糖原增多，从而延长存活期的一个可能原因可能是增加了一种化合物，如丙酮酸，能够氧化NADH。预先暴露的动物的初始丙酮酸高于对照组，注射丙酮酸略微延长了存活时间。
Rats subjected to a brief anoxia can survive 90 sec in a second anoxia, compared to a 60-sec survival time of control animals. Slower disappearance of ATP concentration in the brain during the second exposure indicates this longer survival is due to an altered cerebral energy metabolism. Initial cerebral ATP concentration is no higher in pre-exposed animals than in controls. When glycolysis is inhibited by iodoacetate before testing in anoxia, the advantage of pre-exposure disappears, suggesting the longer survival may be due to increased anaerobic glycolysis. Lactate accumulates faster during anoxia in the brains of pre-exposed animals than in controls, suggesting that increased anaerobic glycolysis is the cause of the prolonged survival. This effect is not due to increased cerebral glucose concentration. A possible reason for this increased glycolysls, and thus the prolonged survival, could be an increase of a compound, such as pyruvate, capable of oxidizing NADH. The initial pyruvate is higher in pre-exposed animals than in controls and injection of pyruvate increases the survival time slightly.