2003 Fiscal Year Final Research Report Summary
The ischemic tolerance induced by electromagnetic field exposure.
| Project/Area Number |
13671625
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Kurume University |
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Principal Investigator |
HARADA Hideki Kurume University, School of Medicine, Assistant Professor, 医学部, 助手 (30198923)
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| Co-Investigator(Kenkyū-buntansha) |
三島 康典 久留米大学, 医学部, 助手 (30258470)
MATSUDA Tsuruo Kurume Institute of Technology, Associate Professor, 知能工学研究所, 助教授 (60258598)
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| Project Period (FY) |
2001 – 2003
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| Keywords | Electromagnetic Fields / Ischemic preconditioning / rats / forebrain ischemia |
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| Research Abstract |
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 mm. Seven days after the ischemic insults, the injury of CA1 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 EME and restraint stress. The Control pretreated with restraint stress followed by 5 and 8 mm 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 mm of ischemia did not protect the CA1 pyramidal cell. By contrast, CA1 pyramidal cells were preserved against 5 mm 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.
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