Tissue injury and hemodynamics in experimental embolic cerebral ischemia

实验性栓塞性脑缺血的组织损伤和血流动力学

基本信息

批准号：
13680816
负责人：
KUROIWA Toshihiko
金额：
$ 2.11万
依托单位：
Tokyo Medical and Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13680816/
关键词：
Cerebral ischemia recirculation Mongolian gerbil C57BI 6J mouse neuronal death Cerebral infarction MRI C57Bl 一過性脳虚血神経脱落症状スナネズミ拡散係数超微細構造

项目摘要

We studied pathophysiological and neurological changes after transient cerebral ischemia induced by by clot embolization and thrombolysis in C57B1/6J mice, and compared the results with a cerebral ischemia induced by temporary ligation of the common carotid artery. Clot embolization and thrombolysis induced a transient CBF decrease for approximately 30 min. Neurological symptoms including spontaneous locomotion and failed grid catching rate was monitored during the observation period of 24 h postischemia. Common carotid artery was temporary ligated to induce cerebral ischemial in gerbil. In mice, frozen brains were processed for mapping of tissue ATP content, Cerebral Protein Synthesis (CPS) and TUNEL staining positive area. In gerbil, we monitored neurological dysfunction for 4 weeks after transient ischemia, and the results were correlated with the histological changes and MRI findings. After clot embolizatin, rCBF reduced to 19.8 +/- 11% of the control level and gradually recovered thereafter. Neurological deficit score gradually became worse during postischemia. The area of CPS reduction was 28.7 +/-11.5% and 38.5 +/- 20.6% of the control at 6 h and 24 h postischemia, respectively. ATP content also reduced to 8.7 +/- 5.4% and 38.4 +/- 22% of the control at 6h and 24h postishemia, respectively. Area of TUNEL positive cells is strikingly similar to the area of CPS reduction at 24 h postischemia. Comparison of the psotischemic changes of neurological and pathophysiological parameters indicate that clot embolization model of cerebral ischemia evolves pathophysiological changes similar to human embolic ischemia and therefore suitable model of experimental cerebral ischemia.

我们研究了C57B1/6J小鼠血栓栓塞和溶栓引起的短暂性脑缺血后的病理生理和神经学变化，并将结果与暂时结扎颈总动脉引起的脑缺血进行了比较。凝块栓塞和溶栓导致 CBF 短暂降低约 30 分钟。在缺血后24小时的观察期内监测神经症状，包括自发运动和网格捕捉失败率。暂时结扎颈总动脉以诱导沙鼠脑缺血。在小鼠中，对冷冻大脑进行处理以绘制组织 ATP 含量、脑蛋白合成 (CPS) 和 TUNEL 染色阳性区域的图谱。在沙鼠中，我们在短暂性缺血后监测神经功能障碍 4 周，结果与组织学变化和 MRI 结果相关。血栓栓塞后，rCBF降至对照水平的19.8+/-11%，此后逐渐恢复。缺血后神经功能缺损评分逐渐恶化。缺血后 6 小时和 24 小时，CPS 减少面积分别为对照的 28.7 +/-11.5% 和 38.5 +/- 20.6%。缺血后 6 小时和 24 小时，ATP 含量也分别降至对照的 8.7 +/- 5.4% 和 38.4 +/- 22%。 TUNEL 阳性细胞的面积与缺血后 24 小时 CPS 减少的面积惊人地相似。脑缺血的神经学和病理生理学参数变化的比较表明，脑缺血的血栓栓塞模型会发生与人类栓塞性缺血相似的病理生理变化，因此适合作为实验性脑缺血模型。