Dweidner A, Betz E, Hohorst H J, Pickerodt V
Acta Neurochir (Wien). 1975;32(3-4):175-98. doi: 10.1007/BF01405452.
Average Po2 and Pco2, local blood flow and pH values in the cerebral cortex of the cat were measured during passive hyperventilation (arterial Pco2 below 19 mm Hg). At defined intervals tissue samples were taken for metabolite analysis. The object of the study was to correlate the data obtained on the brain surface with metabolic responses. Immediately after the start of hyperventilation blood flow decreased, average cortical tissue pressures of O2 and CO2 fell, and there was a simultaneous rise in cortical pH. At a later stage in the experiment the local blood supply reverted to its resting level. Despite a fivefold rise in tissue lactate level during hyperventilation and a decrease in local O2 pressure on the brain surface to 5-10 mm Hg the degree of phosphorylation of energy rich phosphates was not less than under normal conditions of oxygenation. Our investigations showed no evidence of energy lack in cerebral cortex cells during hyperventilation. Cellular hypoxia and its characteristics are defined. The possible causes of raised tissue lactate levels during hyperventilation despite the lack of evidence of cellular hypoxia are discussed.
在被动过度通气(动脉血二氧化碳分压低于19毫米汞柱)期间,测量了猫大脑皮质的平均氧分压和二氧化碳分压、局部血流量及pH值。在规定的时间间隔采集组织样本进行代谢物分析。本研究的目的是将在脑表面获得的数据与代谢反应相关联。过度通气开始后,血流量立即下降,皮质组织氧和二氧化碳的平均压力降低,同时皮质pH值升高。在实验后期,局部血液供应恢复到静息水平。尽管过度通气期间组织乳酸水平升高了五倍,且脑表面局部氧分压降至5 - 10毫米汞柱,但高能磷酸盐的磷酸化程度并不低于正常氧合条件下的水平。我们的研究表明,过度通气期间大脑皮质细胞没有能量缺乏的迹象。定义了细胞缺氧及其特征。讨论了尽管没有细胞缺氧的证据,但过度通气期间组织乳酸水平升高的可能原因。