| Project/Area Number |
09670694
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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 |
Circulatory organs internal medicine
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| Research Institution | Gunma University School of Medicine |
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Principal Investigator |
IMAI Susumu Gunma University , Second Department of Internal Medicine, Assistant, 医学部, 助手 (60184800)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAI Ryozo Gunma University , Second Department of Internal Medicine, Professor, 医学部, 教授 (60207975)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | ageing / acute myocardial infarction / klotho mouse / heat shock protein / SOD / reperfusion / Heat Shock Protein / 再灌流 / 心筋虚血 / HSP |
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| Research Abstract |
<Background> The prognosis of elder patients with acute myocardial infarction is poor. However, its pathophysiological mechanism is not clear and remains to be solved. A new mouse model (the kloth mouse), which shows a syndrome resembling ageing, has recently developed.
<Objective> We investigated whether there are differences in destructive and protective responses to ischemic/reperfused attack between the klotho and wild mouse.
<Methods> After anesthesia and intubation, we occluded the left coronary artery in the klotho mice (n=8) and wild mice (n=8) for 20 minutes and then reperfused for 60 minutes. We measured the myeloperoxidase activity, SOD activity, heat shock protein and TBARS in reperfused myocardium.
<Results> The TBARS in reperfused area, which should indicate oxidative stress after reperfusion, was significantly greater in the klotho mice as compared with that in the wild mice. We found that the ocurrcnce of reperfusion arrhythmia in the klotho mice was significantly greater than in wild mice. With regard to the destructive factor in response to ischemic/reperfused attack, there was no significant difference in myeloperoxidase activity between the two groups. In contrast, both SOD activity and heat shock protein as protective factors in responses to ischemic/reperfused attack were significantly depressed in reperfused area of the klotho mice as compared with the wild mice (P<0.05).
<Conclusion> We found that the reperfusion injury in the klotho mice was significantly greater than that in the wild mice, which may be consistent with the poor prognosis in elder patients with acute myocardial infarction. This may result from the depression of the protective factors such as reduction in SOD activity and heat shock protein production rather than the increase in the destructive factors in responses to ischemic/reperfused attack.
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