Temporary [corrected] cerebral ischemia results in swollen astrocytic end-feet that compress microvessels and lead to delayed [corrected] focal cortical infarction.

Temporary [corrected] cerebral ischemia results in swollen astrocytic end-feet that compress microvessels and lead to delayed [corrected] focal cortical infarction.
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临时[校正]脑缺血会导致星形细胞末端肿胀,从而压缩微丝并导致延迟[校正]局灶性皮质梗塞。

DOI:
10.1038/jcbfm.2010.97
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发表时间:
2011-01
期刊:
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
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其他
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我们研究了暂时性缺血后播散性选择性神经元坏死(DSNN)局灶性梗塞突然发作的机制。根据每隔5小时进行两次左颈动脉闭塞后前10分钟内的中风指数评分选择中风阳性动物。在第二次缺血后的不同时间对动物实施安乐死。光学和电子显微镜研究按时间顺序对大脑皮层的交叉水平的冠状切面进行,其中局灶性梗塞在成熟的 DSNN 中进化。我们计算了神经元、星形胶质细胞和星形胶质细胞突起(AP)的数量;测量末端足和星形胶质细胞的面积;并计数阻塞微血管和炭黑悬浮液灌注微血管(CBSPm)的数量。缺血后0.5~5小时,DSNN成熟,退化和死亡神经元数量增多,APs切端数量减少;而端足面积和阻塞微血管数量增加,而CBSPm减少。缺血后12小时和24小时,梗死进展,​​末足面积和星形胶质细胞数量减少;而阻塞的微血管数量减少,CBSPm 数量增加。局灶性梗塞是由于肿胀的足底受压而导致暂时性微血管阻塞而形成的。
We examined the mechanisms underlying the abrupt onset of the focal infarction in disseminated selective neuronal necrosis (DSNN) after temporary ischemia. Stroke-positive animals were selected according to their stroke-index score during the first 10 minutes after left carotid occlusion performed twice at a 5-hour interval. The animals were euthanized at various times after the second ischemia. Light- and electron-microscopical studies were performed chronologically on the coronal-cut surface of the cerebral cortex at the chiasmatic level, where focal infarction evolved in the maturing DSNN. We counted the number of neurons, astrocytes, and astrocytic processes (APs); measured the areas of end-feet and astrocytes; and counted the numbers of obstructed microvessels and carbon-black-suspension-perfused microvessels (CBSPm). Between 0.5 and 5 hours after ischemia, DSNN matured, with the numbers of degenerated and dead neurons increasing, and those of APs cut-ends decreasing; whereas the area of the end-feet and the numbers of obstructed microvessels increased and those of CBSPm decreased. At 12 and 24 hours after ischemia, the infarction evolved, with the area of end-feet and astrocytic number decreased; whereas the numbers of obstructed microvessels decreased and the CBSPm number increased. The focal infarction evolved by temporary microvascular obstruction because of compression by swollen end-feet.
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