The effect of duration of cerebral ischemia on brain pyruvate dehydrogenase activity, energy metabolites, and blood flow during reperfusion in gerbil brain
The effect of duration of cerebral ischemia on brain pyruvate dehydrogenase activity, energy metabolites, and blood flow during reperfusion in gerbil brain
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DOI：
10.1016/s0006-8993(98)00121-8
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发表时间：
1998-05-04
期刊：
影响因子：
2.9
通讯作者：
Terashi, A
中科院分区：
文献类型：
--
作者：
Fukuchi, T;Katayama, Y;Terashi, A
本研究的目的是确定缺血损伤的持续时间是否影响线粒体酶丙酮酸脱氢酶（PDH）的活性与代谢产物的恢复和区域脑血流量（rCBF）缺血后立即和再灌注期间在沙鼠皮层。脑缺血诱导，使用双侧颈动脉闭塞方法，20或60分钟，然后再灌注120分钟。缺血后立即PDH活性增加三倍，无论缺血时间。缺血60 min组PDH仍处于激活状态，高能磷酸盐的恢复和乳酸的清除较差，再灌注20 min时rCBF为对照组的48%，再灌注120 min时逐渐下降至26%。在20分钟缺血组，PDH活性迅速恢复正常，能量磷酸盐恢复良好，乳酸在再灌注的前60分钟内迅速减少，rCBF在20分钟再灌注时为对照组的65%，在整个再灌注期间保持在对照组的48%以上。在两组中，再灌注后代谢的恢复与rCBF的变化并不平行，在60分钟缺血组中最明显。PDH活性的缓慢正常化反映了60分钟缺血组中代谢物的不良恢复，表明PDH活性在再灌注期间能量代谢物的再合成中是重要的。总之，延长缺血损伤影响再灌注过程中的PDH活性，损害能量代谢产物的恢复，并恶化rCBF的恢复。(C)1998年Elsevier Science B.V.
The objective of this study was to determine whether the duration of an ischemic insult effects the activity of the mitochondrial enzyme pyruvate dehydrogenase (PDH) in relation to the recovery of metabolites and regional cerebral blood flow (rCBF) immediately after ischemia and during reperfusion in gerbil cortex. Cerebral ischemia was induced, using the bilateral carotid artery occlusion method, for 20 or 60 min, followed by reperfusion up to 120 min. Immediately after ischemia PDH activity increased threefold regardless of ischemic duration. In the 60-min ischemic group, PDH remained activated, the recovery of high energy phosphates and the clearance of lactate were poor, and the rCBF was 48% of controls after 20-min reperfusion, decreasing gradually to 26% at 120-min reperfusion. In the 20-min ischemic group, PDH activity normalized quickly, the restoration of energy phosphates was good, there was a quick reduction in lactate within the first 60 min of reperfusion, and the rCBF was 65% of control at 20-min reperfusion, and remained over 48% of control throughout reperfusion. Recovery of metabolism after reperfusion did not parallel the changes in rCBF in either group, most noticeably in the 60-min ischemic group. The slow normalization of PDH activity reflected the poor recovery of metabolites in the 60-min ischemic group, indicating that PDH activity is important in the resynthesis of energy metabolites during reperfusion. In conclusion, prolonging the ischemic insult effected PDH activity during reperfusion, impaired recovery of energy metabolites, and worsened the recovery of rCBF. (C) 1998 Elsevier Science B.V.