LaManna J C, Griffith J K, Cordisco B R, Bell H E, Lin C W, Pundik S, Lust W D
Department of Neurology, Case Western Reserve University, School of Medicine, Cleveland, OH 44106, USA.
Brain Res. 1995 Jul 31;687(1-2):175-81. doi: 10.1016/0006-8993(95)00516-s.
We studied the intracellular pH in rat cerebral cortex of rats subjected to reversible total cerebral ischemia by cardiac arrest and resuscitation. Brain acidoses was more pronounced during ischemia in hyperglycemic rats (6.21 +/- 0.14) than in normoglycemic rats (6.56 +/- 0.07). Brain tissue lactate accumulated proportionally. Nevertheless, within 5 min of reperfusion, pHi in both normoglycemic and hyperglycemic groups had recovered to baseline levels, i.e. near 7.1-7.2, despite the fact that lactate concentrations were still elevated. These results demonstrate a rapid reversal of ischemic acidosis during recovery from 10 min of cardiac arrest, and suggest that acidosis, per se, may not be responsible for neuronal damage following cardiac arrest and resuscitation, even in hyperglycemic conditions.
我们研究了通过心脏停搏和复苏导致可逆性全脑缺血的大鼠大脑皮质中的细胞内pH值。高血糖大鼠缺血期间脑酸中毒(6.21±0.14)比正常血糖大鼠(6.56±0.07)更明显。脑组织乳酸按比例积累。然而,再灌注5分钟内,正常血糖和高血糖组的细胞内pH值均已恢复至基线水平,即接近7.1 - 7.2,尽管乳酸浓度仍升高。这些结果表明,在心脏停搏10分钟后的恢复过程中,缺血性酸中毒迅速逆转,并提示酸中毒本身可能并非心脏停搏和复苏后神经元损伤的原因,即使在高血糖情况下也是如此。