Dynamic changes in cortical NADH fluorescence and direct current potential in rat focal ischemia: Relationship between propagation of recurrent depolarization and growth of the ischemic core
Dynamic changes in cortical NADH fluorescence and direct current potential in rat focal ischemia: Relationship between propagation of recurrent depolarization and growth of the ischemic core
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DOI：
10.1097/00004647-200201000-00009
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发表时间：
2002-01-01
影响因子：
6.3
通讯作者：
Hirakawa, M
中科院分区：
文献类型：
--
作者：
Higuchi, T;Takeda, Y;Hirakawa, M
40只大鼠通过闭塞左侧大脑中动脉和左侧颈总动脉进行3小时的局灶性缺血。通过用紫外线照射顶叶皮质，使用直流电位和 NADH（还原型烟酰胺腺嘌呤二核苷酸）荧光图像分析缺血核心周围反复去极化的传播。根据直流记录部位的组织学评估，导致 50% 神经元损伤的去极化总时间估计为 18.2 分钟。由于去极化时间短，显示反复去极化的部位导致 23 +/- 29% 的神经元损伤，而显示反复去极化并最终持续去极化的部位导致梗死。 NADH 荧光图像显示反复的去极化沿着缺血核心的边缘传播。在85.9%的反复去极化中，荧光消失，不留任何痕迹，并且不影响缺血核心区域。然而，在 47.5% 的动物中，14.1% 的复发性去极化与缺血核心合并，并使面积增加 6 +/- 4 mm(2)。这些研究结果表明，反复去极化会增加神经元损伤的严重程度，但如果不进行持续去极化，其本身不会引起梗塞，并且持续去极化的面积会扩大，14.1%的反复去极化。
Forty rats were subjected to 3 hours of focal ischemia by occluding the left middle cerebral and left common carotid arteries. The propagation of recurrent depolarization around the ischemic core was analyzed using direct-current potential and NADH (reduced nicotinamide adenine dinucleotide) fluorescence images by irradiating the parietal-temporal cortex with ultraviolet light. Based on histological evaluation at direct-current recording sites, the total time of depolarization causing 50% neuronal injury was estimated to be 18.2 minutes. The sites showing recurrent depolarizations resulted in 23 +/- 29% neuronal injury due to the short depolarization time, whereas the sites showing recurrent depolarizations and eventually persistent depolarization resulted in infarction. The NADH fluorescence images showed that recurrent depolarizations propagated along the margin of the ischemic core. In 85.9% of the recurrent depolarizations, the fluorescence disappeared without leaving any traces and did not affect the area of the ischemic core. However, in 47.5% of the animals, 14.1% of recurrent depolarizations merged with the ischemic core and increased the area by 6 +/- 4 mm(2). These findings suggest that recurrent depolarization increases the severity of neuronal injury but does not cause infarction by itself if persistent depolarization does not follow, and that the area of persistent depolarization is enlarged with 14.1% of recurrent depolarizations.