TRANSITION FROM ISCHEMIC NEURONAL NECROSIS TO INFARCTION IN REPEATED ISCHEMIA

TRANSITION FROM ISCHEMIC NEURONAL NECROSIS TO INFARCTION IN REPEATED ISCHEMIA
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DOI:
10.1016/0006-8993(95)00449-z
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发表时间:
1995-07-17
期刊:
影响因子:
2.9
通讯作者:
YOSHIDA, M
YOSHIDA, M
中科院分区:
医学3区
文献类型:
--
作者:
HANYU, SJ;ITO, U;YOSHIDA, M

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为了研究反复缺血后皮层的形态学变化,在沙鼠中以6小时的间隔对颈动脉进行一次、两次和三次7分钟的单侧闭塞,以12小时的间隔对颈动脉进行三次、四次和五次7分钟的类似闭塞。动物与一个和两个7分钟闭塞在6小时的时间间隔显示选择性神经元坏死的皮质,那些与三个7分钟闭塞在6小时的时间间隔显示局灶性梗死在第三层的皮质。3个7分钟闭塞在12小时的时间间隔的动物表现出选择性神经元坏死,那些4个7分钟闭塞在12小时的时间间隔显示局灶性梗死的第三层。在5个7分钟闭塞在12小时的时间间隔的动物,梗死影响皮层的所有层。本研究的结果表明,皮质梗死发生时,短暂的缺血性损伤,不造成任何可见的形态学损伤的皮质神经元反复造成的,并在皮层梗死的发展反复发作缺血依赖于两个侮辱的数量和它们之间的时间间隔。这一发现表明,反复缺血有一个梗死阈值。在我们的模型中,缺血性脑损伤的各个阶段可以更容易地实现比在短暂性缺血损伤的数量或它们之间的间隔。该模型适用于研究缺血性神经元坏死向梗死转化的病理生理过程。
To study morphological changes in the cortex that follow repeated ischemia, one, two, and three 7-min unilateral occlusions of the carotid artery at 6-h intervals, and three, four, and five 7-min similar occlusions at 12-h intervals were produced in gerbils. Animals with one and two 7-min occlusions at 6-h intervals showed selective neuronal necrosis in the cortex; those with three 7-min occlusions at 6-h intervals showed focal infarction in the third layer of the cortex. Animals with three 7-min occlusions at 12-h intervals showed selective neuronal necrosis; those with four 7-min occlusions at 12-h intervals showed focal infarction in the third layer. In animals with five 7-min occlusions at 12 h intervals, infarction affecting all layers of the cortex was seen. Results of the present study indicate that cortical infarction occurred when a brief ischemic insult that does not cause any visible morphological damage in cortical neurons was inflicted repeatedly, and that development of infarction in the cortex following repeated episodes of ischemia depended on both the number of insults and the time intervals between them. This finding suggests that there is a threshold of infarction in repeated ischemia. In our model, various stages of ischemic brain injury could be achieved more easily than in transient ischemia by altering the number of insults or the intervals between them. This model is suitable for studying the pathophysiology on transition from ischemic neuronal necrosis to infarction.