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The ischemic tolerance induced by transcranial magnetic stimulation

经颅磁刺激诱导的缺血耐受

基本信息

批准号：
11671531
负责人：
HARADA Hideki
金额：
$ 0.64万
依托单位：
Kurume University, School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671531/
关键词：
Electromagnetic Fields Ischemic preconditioning rats forebrain ischemia 細胞内カルシウム

项目摘要

Introduction : It has been suggested that magnetic field promotes the Heat Shock Protein 70 gene expression and synthesis, could cause a rapid induction of the immediate-early genes known to play one of the major roles in acquisition of ischemic preconditioning in the central nervous system. In this study we have tested in rats the hypothesis that electromagnetic field (EMF) could make neurons more tolerant to subsequent lethal forebrain ischemia. Materials and Methods : Wistar rats were randomly allocated to one of six experimental groups. Sham animals with restraint stress and EM field exposure were subjected to sham operation. Non-stimulated (Control) and stimulated groups with 8 Hz, 25 Hz and 50 Hz of EMF (2mT) were subjected to lethal forebrain ischemia at 2 days after pretreatment. The brain ischemia was achieved by 4-vessel occlusion technique and was applied for 5 or 8 min. Seven days after the ischemic insults, the injury of CA 1 neurons was examined in coronal planes 3.3-mm posterior to the bregma. Through light microscopic examination, viable and nonviable neurons were counted manually in a double-blinded fashion. Results : The CA1 sector was not damaged at all by pretreatment with EMF and restraint stress. The Control pretreated with restraint stress followed by 5 and 8 min of ischemia produced moderate to severe reduction in the CA1 pyramidal cells depending on the length of ischemia respectively. The pretreatment with EMF followed by 8 min of ischemia did not protect the CA1 pyramidal cell. By contrast, CA1 pyramidal cells were preserved against 5 min of ischemia in animals pretreated with EMF of 25 Hz but not preserved with EMF of 8 and 50 Hz. Conclusion : The data suggest that EMF at 2 days before ischemia have a possibility to reduce potential effect on the reduction of subsequent mild ischemic brain damage.

简介：研究表明，磁场可促进热休克蛋白70基因的表达和合成，并可快速诱导在中枢神经系统获得缺血预适应中起主要作用的即刻早期基因。在这项研究中，我们在大鼠中测试了电磁场（EMF）可以使神经元更耐受随后的致死性前脑缺血的假设。材料与方法：Wistar大鼠随机分为6个实验组。假手术组动物在束缚应激和电磁场暴露下进行假手术。非刺激组（对照组）和8Hz、25 Hz和50 Hz电磁场（2 mT）刺激组在预处理后2天进行致死性前脑缺血。采用4-血管闭塞技术造成脑缺血，缺血时间为5或8 min。缺血后7 d，在冠状面前囟后3.3 mm处检查CA 1神经元的损伤情况。通过光学显微镜检查，以双盲方式手动计数存活和非存活神经元。结果：电磁场预处理和束缚应激对海马CA 1区无明显损伤。对照组在束缚应激后分别缺血5 min和8 min，根据缺血时间的长短，CA 1区锥体细胞分别出现中度至重度减少。电磁场预处理再缺血8 min对海马CA 1区锥体细胞无保护作用。相比之下，CA 1锥体细胞保存对5分钟的缺血预处理与EMF的25 Hz的动物，但不保存与EMF的8和50 Hz。结论：这些数据表明，在缺血前2天的电磁场有可能减少对减少随后的轻度缺血性脑损伤的潜在影响。