Mabe H, Blomqvist P, Siesjö B K
J Cereb Blood Flow Metab. 1983 Mar;3(1):109-14. doi: 10.1038/jcbfm.1983.13.
The objective of the present study was to discover whether or not intracellular alkalosis develops in the brain in the recovery period following transient ischemia. Forebrain ischemia of 15-min duration was induced by four-vessel occlusion in rats, with recovery periods of 15, 60, and 180 min. Intracellular pH was derived both by the HCO3- -H2CO3 method and from the creatine kinase equilibrium. The ischemia was associated with energy failure and marked accumulation of lactic acid in the cerebral cortex. Recirculation brought about rapid rephosphorylation of adenine nucleotides and gradual normalization of lactic acid levels. After 15 min of recovery, the HCO3- -H2CO3 method indicated persisting acidosis, but the creatine kinase reaction did not. After 60 min, a shift of pH in the alkaline direction was demonstrated in both methods. This alkalosis had disappeared after 3 h of recovery. It is concluded that resumption of ATP production after ischemia is followed by a rapid rise in intracellular pH, which transiently increases above normal.
本研究的目的是探究在短暂性脑缺血后的恢复期，大脑中是否会发生细胞内碱中毒。通过四动脉闭塞法诱导大鼠进行持续15分钟的前脑缺血，恢复期分别为15分钟、60分钟和180分钟。采用HCO₃⁻ - H₂CO₃法和肌酸激酶平衡法测定细胞内pH值。缺血与能量衰竭以及大脑皮质中乳酸的大量积累有关。再灌注导致腺嘌呤核苷酸迅速重新磷酸化，乳酸水平逐渐恢复正常。恢复15分钟后，HCO₃⁻ - H₂CO₃法显示仍存在酸中毒，但肌酸激酶反应未显示。60分钟后，两种方法均显示pH值向碱性方向转变。这种碱中毒在恢复3小时后消失。结论是缺血后ATP生成恢复后，细胞内pH值迅速升高，并短暂高于正常水平。
