Nemoto E M, Frinak S
Stroke. 1981 Jan-Feb;12(1):77-82. doi: 10.1161/01.str.12.1.77.
Studies were done on rats to determine whether thiopental loading after complete, transient, global brain ischemia causes more rapid postischemic normalization of brain tissue pH. Fifteen halothane-anesthetized rats were subjected to 16 min of complete global brain ischemia by a combination of systemic arterial hypotension (40 torr) and a high pressure (1500 torr) neck cuff. Brain tissue pH was continuously monitored for up to 2 hour postischemia with microelectrodes (tip diameters of one to two micrometers) inserted about 500 micrometers into the parietal cortex. During ischemia, brain pH fell rapidly within the first 5 min from 7.0 to 6.2 and changed little thereafter. With restoration of arterial pressure and deflation of the neck cuff, pH did not immediately begin to rise back towards normal. Instead, after a few minutes, it transiently fell to even lower values before beginning to increase indicating increased tissue lactic acidosis when the brain is resaturated with glucose upon reperfusion. Beginning at 5 min postischemia, 7 of the 15 rats were infused with thiopental (90 mg/kg, IV over 60 min). At 30 min postischemia, brain tissue pH was similar in both groups and by 60 min, back to preischemic values. We conclude that thiopental loading postischemia does not improve normalization of brain pH. The transient decrease in brain pH with reperfusion is discussed.
对大鼠进行了研究,以确定在完全性、短暂性全脑缺血后给予硫喷妥钠负荷是否能使脑组织pH值在缺血后更快恢复正常。15只接受氟烷麻醉的大鼠通过全身动脉低血压(40托)和高压(1500托)颈套相结合的方式经历16分钟的完全性全脑缺血。在缺血后长达2小时内,用插入顶叶皮质约500微米处的微电极(尖端直径为1至2微米)连续监测脑组织pH值。在缺血期间,脑pH值在最初5分钟内迅速从7.0降至6.2,此后变化不大。随着动脉压恢复和颈套放气,pH值并没有立即开始回升至正常。相反,几分钟后,它短暂降至更低值,然后才开始上升,这表明在再灌注时大脑重新充满葡萄糖时组织乳酸酸中毒加剧。缺血后5分钟开始,15只大鼠中有7只被注入硫喷妥钠(90毫克/千克,静脉注射,60分钟内)。缺血后30分钟,两组的脑组织pH值相似,到60分钟时,恢复到缺血前的值。我们得出结论,缺血后给予硫喷妥钠负荷并不能改善脑pH值的恢复正常。文中讨论了再灌注时脑pH值的短暂下降。