Effects of anoxia on cerebral metabolism and electrolytes in man
Effects of anoxia on cerebral metabolism and electrolytes in man
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缺氧对人脑代谢和电解质的影响
DOI：
10.1212/wnl.15.10.892
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发表时间：
1965
期刊：
影响因子：
9.9
通讯作者：
M. Tomita
中科院分区：
文献类型：
--
作者：
J. Meyer;F. Gotoh;S. Ebihara;M. Tomita
脑组织的氧张力（PO,）遵循供需规律。供应受动脉血氧含量、脑血流量和脑血pH值（受玻尔效应）的影响，而需求完全取决于脑代谢的功能状态。如果血液的氧张力降低（例如，通过缺氧吸入氮），可能会达到一个值，低于毛细血管PO，不足以维持氧气扩散到脑组织；会导致脑缺氧症状的功能损害。这样的氧张力阈值已被确定用于脑制剂；在此水平以下，脑氧消耗降低，脑静脉PO阈值（脑电图减慢和脑代谢降低）也被一些研究者估计。1-5除了在氮气呼吸和体位性低血压时发生意识丧失的颈内静脉血氧饱和度水平的一些测定外，目前还没有可比较的人类数据在动物实验中有报道，当组织或毛细血管静脉pOz在诱导缺氧时低于阈值时，脑细胞外钠离子减少，细胞外钾离子增加。这种离子变化据说与脑电图减慢有关。5,7rs这些数据支持了缺氧症状和体征是由于脑内活性钠转运机制的失败，这显然依赖于脑能代谢。本研究首次在人类中报道了关于脑静脉氧张力阈值的类似观察结果
THE OXYGEN tension (PO,) of brain tissue obeys the law of supply and demand. Supply is influenced by arterial oxygen content, cerebral blood flow, and cerebral blood pH (by the Bohr effect), and demand depends soleIy on the functional state of brain metabolism. If the oxygen tension of the blood is reduced (for example, by anoxic anoxia of nitrogen inhalation), presumably a value will be reached below which capillary PO, is insufficient to maintain oxygen diffusion into brain tissue; functional impairment with signs of cerebral anoxia will result. Such thresholds for oxygen tension have been determined for brain preparations; below these cerebral oxygen consumption became decreased and thresholds for cerebral venous PO,-at which electroencephalographic slowing and decreased cerebral metabolism occurred-have also been estimated in animals by several investigators.1-5 There is as yet no comparable data available in man except a few determinations of the levels of oxygen saturation in the internal jugular vein at which loss of consciousness occurred during nitrogen breathing and postural hypotension.6 It has been reported in animals that when tissue or capillary venous pOz fell below threshold during induced anoxia the extracellular sodium ions of the brain decreased and there was an increase of extracellular potassium. This ionic change was said to correlate with electroencephalographic slowing.5,7rs Such data support the notion that anoxic symptoms and signs are due to failure of the mechanism for active sodium transport in brain, which is apparently dependent on cerebral energy metabolism. The present study reports for the first time in man similar observations concerning the threshold for cerebral venous oxygen tension