Regional differences in the rate of energy impairment after threshold level ischemia for induction of cerebral infarction in gerbils
Regional differences in the rate of energy impairment after threshold level ischemia for induction of cerebral infarction in gerbils
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DOI：
10.1007/s004010000235
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发表时间：
2000-12-01
影响因子：
12.7
通讯作者：
Ito, U
中科院分区：
文献类型：
--
作者：
Kuroiwa, T;Mies, G;Ito, U
短暂性脑缺血后脑梗塞和/或选择性神经元死亡的发展取决于缺血发作的严重程度。短暂性脑缺血达到诱导脑梗塞的阈值水平后，这两种变化在脑缺血后各区域缓慢演变。我们研究了脑缺血后不同区域能量代谢紊乱与脑梗塞和选择性神经元死亡的关系。我们的结果表明，在发生脑梗塞的不同脑区，组织中的ATP含量与琥珀酸脱氢酶活性平行，在恢复循环后的4天内，在不同的时间降至最低水平(从早到晚：丘脑背外侧核和GT；背外侧尾状核和GT；视交叉水平皮质和GT；海马CA3区和GT区)。在漏斗水平的皮质，在恢复循环后的7天内出现播散性选择性神经元死亡；伴随而来的只是能量代谢的轻微改变。结果表明，沙土鼠脑缺血后能量受损和进展性脑梗塞的发生率存在区域差异。与线粒体酶功能障碍相关的能量损伤似乎是脑梗塞延迟表现所必需的，但对播散性选择性神经元死亡不是必需的。
The development of infarction and/or selective neuronal death in the brain after transient cerebral ischemia depends on the severity of the ischemic episode. After transient cerebral ischemia of the threshold level for the induction of infarction, both changes evolve slowly in various postischemic regions. We examined the relationship of disturbances of energy metabolism to infarction and selective neuronal death in various regions of the postischemic brain subjected to two 10-min occlusions of the unilateral common carotid artery. Our results indicated that in various cerebral regions that developed infarction, the tissue ATP content, in parallel with the succinic dehydrogenase activity, fell to their lowest levels at different times over a 4-day period after circulation had been restored (earliest to latest: dorsolateral thalamus > dorsolateral caudate > chiasmal level cortex > hippocampal CA3 sector > hippocampal CAI sector). In the cortex at the infundibular level, disseminated selective neuronal death developed over a 7-day period following restoration of circulation; it was accompanied by only a slight alteration in energy metabolism. The present results indicate that regional differences existed in the rate of energy impairment and evolving infarction in the postischemic gerbil brain. Energy impairment, in association with mitochondrial enzymatic dysfunction, seems to be indispensable for the delayed manifestation of cerebral infarction but not for disseminated selective neuronal death.