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：已经提出，磁场促进热激蛋白70基因表达和合成，可能会迅速诱导已知的直接天气基因在中枢神经系统中扮演缺血预处理的主要作用之一。在这项研究中，我们在大鼠中测试了电磁场（EMF）可以使神经元对随后的致命性前脑缺血更耐受的假设。材料和方法：将Wistar大鼠随机分配给六个实验组之一。具有约束应力和EM场暴露的假动物进行假手术。预处理后2天，对具有8 Hz，25 Hz和50 Hz EMF（2MT）的非刺激组和50 Hz的EMF（2MT）进行了致命的前脑缺血。脑部缺血是通过4个血管闭塞技术实现的，并应用了5或8分钟。缺血性损伤7天后，在冠状动脉3.3毫米的冠状平面上检查了Ca 1神经元的损伤。通过轻微的显微镜检查，以双盲方式手动计数可行和不可生存的神经元。结果：通过用EMF和约束应力进行预处理，CA1部门根本没有损坏。用约束应力预处理的对照，然后是5分钟和8分钟的缺血，分别根据缺血的长度而在CA1锥体细胞中中度至严重降低。用EMF进行预处理，然后进行8分钟的缺血并不能保护CA1锥体细胞。相比之下，用EMF预处理的25 Hz预处理但不保留EMF为8和50 Hz的动物，将CA1锥体细胞与5分钟的缺血保留。结论：数据表明，缺血前2天的EMF有可能减少对随后轻度缺血性脑损伤减少的潜在影响。