Ischemic tolerance after spinal cord ischemia

脊髓缺血后的缺血耐受

基本信息

批准号：
09671567
负责人：
MATSUMOTO Mishiya
金额：
$ 1.98万
依托单位：
Yamaguchi University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09671567/
关键词：
spinal cord ischemia tolerance heat shock protein rabbit

项目摘要

We investigated the effect of interval between brief spinal cord ischemia and subsequent severe ischemic insult on hindlimb motor function and histopathology of the spinal cord. To explore the mechanism of spinal ischemic tolerance, induction of 70- kDa heat shock protein (HSP70) was also evaluated.A brief spinal cord ischemia was produced by occlusion of the abdominal aorta during isoflurane anesthesia. Recirculation after brief ischemia was started when the third negative wave of segmental spinal cord evoked potential disappeared. This ischemic insult did not produce neuronal damage in the spinal cord. Two days, 4 days, or 7 days (n=8 in each) following the first ischemia, the animals (double ischemia group) were subjected to the second ischemia for 20 minutes. The single ischemia group received a sham procedure instead of the first ischemia and was identically subjected to the second ischemia 4 days following the sham procedure. Two days following the second ischemia, hindlimb motor function was evaluated. After perfusion and fixation of the spinal cord, normal neurons in the anterior lumber spinal cord were counted.The neurologic status and histopathology in the animals in the double ischemia group subjected to the second ischemia 4 days after first ischemia were significantly better than in the single ischemia group. HSP70 was induced 2 days, 4 days, and 7 days after brief spinal cord ischemia. Intense HSP70 staining was observed 4 hours after second ischemic insult in all animals that showed normal neurologic function regardless of preconditioning with brief spinal cord ischemia.These results suggest that ischemic tolerance was observed 4 days, but not adequately 2 or 7 days after brief spinal cord ischemia and that factors other than HSP70 may play an important role in the mechanism of spinal ischemic tolerance.

我们研究了短暂脊髓缺血和随后的严重缺血性损伤之间的间隔对后肢运动功能和脊髓组织病理学的影响。为了探讨脊髓缺血耐受的机制，还评估了70-kDa热休克蛋白(HSP70)的诱导。在异氟醚麻醉期间通过闭塞腹主动脉产生短暂的脊髓缺血。当节段性脊髓诱发电位的第三个负波消失时，短暂缺血后开始再循环。这种缺血性损伤不会造成脊髓神经元损伤。第一次缺血后两天、四天或七天(各n＝8)，使动物(双次缺血组)进行第二次缺血20分钟。单次缺血组接受假手术代替第一次缺血，并在假手术后4天同样进行第二次缺血。第二次缺血两天后，评估后肢运动功能。脊髓灌注固定后，对前腰部脊髓正常神经元进行计数。第一次缺血4天后进行第二次缺血的双次缺血组动物的神经状态和组织病理学明显优于单次缺血组。缺血组。在短暂脊髓缺血后2天、4天和7天诱导HSP70。在第二次缺血性损伤后 4 小时，在所有表现出正常神经功能的动物中观察到强烈的 HSP70 染色，无论是否进行短暂脊髓缺血预处理。这些结果表明，在短暂脊髓缺血 4 天后观察到缺血耐受性，但在短暂脊髓缺血后 2 或 7 天观察到的缺血耐受性不充分。研究表明，HSP70 以外的因素可能在脊髓缺血耐受机制中发挥重要作用。