Potassium ion homeostasis and mitochondrial redox activity in brain: relative changes as indicators of hypoxia.
Potassium ion homeostasis and mitochondrial redox activity in brain: relative changes as indicators of hypoxia.
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大脑中钾离子稳态和线粒体氧化还原活性：作为缺氧指标的相对变化。
DOI：
10.1038/jcbfm.1988.44
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Sick,TJ
中科院分区：
文献类型：
--
作者：
Milito,SJ;Raffin,CN;Rosenthal,M;Sick,TJ
本研究旨在研究缺氧时离子转运和线粒体氧化还原活性的关系，作为确定脑氧充足的一步。为此，在戊巴比妥麻醉大鼠的大脑皮层中，用离子选择性微电极记录细胞外钾离子活性（K+o），同时用反射分光光度法监测细胞色素氧化酶（cytochromea,a3）的还原/氧化（氧化还原）比率。在常氧条件下，直接皮层刺激神经元激活产生细胞染色质、a3的短暂氧化和K+o的升高。中度缺氧（pao2高于50 mm Hg）导致细胞色素减少，但K+o仅轻微升高。在这种低氧水平下，细胞染色质a3继续响应神经元的激活，瞬间向氧化方向转移，K+o再积累的速率与对照组相比没有变化。当pao2进一步降低到临界阈值以下时，刺激引起的线粒体反应物氧化反应被转向还原所取代，但通过神经元激活溢出到细胞外空间的K+再积累速率保持不变。只有在严重缺氧时（pao2低于20 mm Hg），一些动物才有可能在不引起弥漫性皮质抑制的情况下减慢K+o的再积累。这些数据表明，与线粒体氧化还原功能相比，大脑皮层的离子转运活性对缺氧的抵抗力更强。他们提出了一种与体外线粒体的“缓冲”作用相似的体内效应，尽管氧合和氧化还原比率波动，但在体内氧气消耗保持不变，而且哺乳动物大脑中为离子运输提供能量的厌氧能力可能比以前所认识到的要大。
This study was directed at relating ion transport and mitochondrial redox activity during hypoxia, as a step toward definition of brain oxygen sufficiency. To accomplish this, extracellular potassium ion activity (K+o) was recorded by ion-selective microelectrodes while reduction/oxidation (redox) ratios of cytochrome oxidase (cytochromea,a3) were monitored by reflection spectrophotometry in cerebral cortex of rats anesthetized with pentobarbital. In normoxia, neuronal activation by direct cortical stimulation produced transient oxidation of cytochromea,a3and elevation of K+o. Moderate hypoxia (Pao2above 50 mm Hg) resulted in reduction of cytochromea,a3but only slight elevation of K+o. At this level of hypoxia, cytochromea,a3continued to respond to neuronal activation with transient shifts toward oxidation and rates of K+o reaccumulation were unchanged from control. When Pao2was further decreased below a critical threshold, stimulus-provoked oxidative responses of mitochondrial reactants were replaced by shifts toward reduction, but rates of reaccumulation of K+, spilled into the extracellular space by neuronal activation, remained unchanged. Only during severe hypoxia (Pao2less than 20 mm Hg) was it possible in some animals to record a slowing in the reaccumulation of K+o without provocation of spreading cortical depression. These data indicate that ion transport activity in cerebral cortex is more refractory to hypoxia than is mitochondrial redox functioning. They suggest an in vivo parallel to the “cushioning” effect of mitochondria in vitro, in which oxygen consumption remains constant despite fluctuations in oxygenation and redox ratios, and also that there may be a greater anaerobic capacity to provide energy for ion transport in mammalian brain than has previously been appreciated.