Very delayed infarction after mild focal cerebral ischemia: A role for apoptosis?
Very delayed infarction after mild focal cerebral ischemia: A role for apoptosis?
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DOI：
10.1097/00004647-199603000-00003
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发表时间：
1996-03-01
影响因子：
6.3
通讯作者：
Choi, DW
中科院分区：
文献类型：
--
作者：
Du, C;Hu, R;Choi, DW
观察颈总动脉和右大脑中动脉短暂性闭塞大鼠脑梗死的时间演变。严重（90分钟）缺血后，6小时内出现明显的右侧皮质梗死，1天后完全发展。轻度（30分钟）缺血后，1天后未出现皮质梗死。然而，3天后发生梗死；2周时，梗死体积与缺血90 min时相当。这些数据表明，轻度局灶性缺血后的梗死可以令人惊讶的延迟方式发展。一些证据表明，严重缺血后存在神经元凋亡，但仅在有限程度上。然而，轻度缺血3天后，成熟梗死边缘的神经元显示明显的TUNEL染色，从缺血皮质梗死周围区域制备的DNA显示核小体间断裂。此外，1 mg/kg环己亚胺预处理在轻度缺血2周后显著减少梗死体积。这些数据提出了一种可能性，即依赖于活性蛋白合成的细胞凋亡有助于轻度短暂性局灶性脑缺血大鼠观察到的延迟梗死。
The temporal evolution of cerebral infarction was examined in rats subjected to transient occlusion of both common carotid arteries and the right middle cerebral artery. After severe (90-min) ischemia, substantial right-sided cortical infarction was evident within 6 h and fully developed after 1 day. After mild (30-min) ischemia, no cortical infarction was present after 1 day. However, infarction developed after 3 days; by 2 weeks, infarction volume was as large as that induced by 90-min ischemia. These data suggest that infarction after mild focal ischemia can develop in a surprisingly delayed fashion. Some evidence of neuronal apoptosis was present after severe ischemia, but only to a limited degree. However, 3 days after mild ischemia, neurons bordering the maturing infarction exhibited prominent TUNEL staining, and DNA prepared from the periinfarct area of ischemic cortex showed internucleosomal fragmentation. Furthermore, pretreatment with 1 mg/kg cycloheximide markedly reduced infarction volume 2 weeks after mild ischemia. These data raise the possibility that apoptosis, dependent on active protein synthesis, contributes to the delayed infarction observed in rats subjected to mild transient focal cerebral ischemia.