TEMPORAL THRESHOLDS FOR NEOCORTICAL INFARCTION IN RATS SUBJECTED TO REVERSIBLE FOCAL CEREBRAL-ISCHEMIA
TEMPORAL THRESHOLDS FOR NEOCORTICAL INFARCTION IN RATS SUBJECTED TO REVERSIBLE FOCAL CEREBRAL-ISCHEMIA
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DOI：
10.1161/01.str.22.8.1032
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发表时间：
1991-08-01
期刊：
影响因子：
8.3
通讯作者：
PULSINELLI, W
中科院分区：
文献类型：
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作者：
KAPLAN, B;BRINT, S;PULSINELLI, W
我们研究了自发性高血压大鼠局灶性脑梗死的时间阈值。分别阻断右侧大脑中动脉和颈总动脉0、1、2、3、4、24小时，缺血24小时后处死。通过图像分析，对苏木精和伊红染色组织的连续冷冻切片进行皮质梗死体积和水肿体积的量化。闭塞后，用激光多普勒血流仪测量缺血区核心血流，平均+/-标准差为闭塞前基线值的21 +/- 7% （n = 26）。在缺血的第一个小时，密集缺血区的血流量上升到基线的27 +/- 8% （n = 25）。释放大脑中动脉和颈总动脉闭塞后，皮质血流量迅速恢复到基线的213 +/- 83% （n = 21）。局灶性缺血持续1小时，很少或不引起梗死，而缺血间隔2和3小时，皮层梗死体积依次增大。缺血间隔3-4小时，再循环约20小时，梗死面积与24小时永久性局灶性缺血后的梗死面积无显著差异。结果表明，该大鼠模型局灶性脑缺血3-4小时足以达到最大梗死，并提示在此时间后再循环或药物干预将收效甚微。
We investigated the temporal threshold for focal cerebral infarction in the spontaneously hypertensive rat. The right middle cerebral artery and common carotid artery were occluded for 0,1 2,3,4, or 24 hours, and all the animals were sacrificed 24 hours after the onset of ischemia. Cortical infarct volumes and edema volumes were quantified in serial frozen sections of hematoxylin and eosin-stained tissue using image analysis. Upon occlusion, blood flow in the core of the ischemic zone, measured with laser-Doppler flowmetry, fell to a mean +/- standard deviation of 21 +/- 7% of the preocclusion baseline value (n = 26). During the first hour of ischemia, blood flow in the densely ischemic zone rose to 27 +/- 8% of baseline (n = 25). Release of the middle cerebral artery and common carotid artery occlusions rapidly restored cortical blood flow to 213 +/- 83% of baseline (n = 21). Focal ischemia of 1 hour's duration caused little or no infarction, while ischemic intervals of 2 and 3 hours produced successively larger volumes of infarcted cortex. Ischemic intervals of 3-4 hours' duration followed by approximately 20 hours of recirculation yielded infarct volumes that were not significantly different from those after 24 hours of permanent focal ischemia. The results indicate that 3-4 hours of focal cerebral ischemia in this rat model is sufficient to attain maximal infarction and suggest that recirculation or pharmacological interventions after this time will provide little benefit.