| Project/Area Number |
12670710
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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 | Fukuoka University |
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Principal Investigator |
IDEISHI Munehito School of medicine, Fukuoka University Professor, 医学部, 教授 (20131807)
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| Co-Investigator(Kenkyū-buntansha) |
KUMAGAI Koichiro School of Medicine, Fukuoka University Lecturer, 医学部, 講師 (10248510)
SAKU Keijirou School of Medicine, Fukuoka University Professor, 医学部, 教授 (40183371)
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| Project Period (FY) |
2000 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
|
| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | myocardial ischemia / angiotensin / ischemia / reperfusion / apoptosis / myocardial infarction / oxidative stress / 酸化ストレス |
|---|
| Research Abstract |
1. Ischemia/reperfusion-induced arrhythmias in anesthetized rats were suppressed by the administration of angiotensin II type 1 receptor antagonist (ATI-A) or angiotensin converting enzyme inhibitor (ACE-I). The effect of ACE-I was not reversed by the co-administration of bradykinin B2 receptor antagonist. Calcium exchanger inhibitor or L-type Calcium channel inhibitor was more efficiently suppressed the arrhythmias than ATI antagonist or ACE-I. Superoxide dismutase did not show any antiarrhythmic effects in this model.
2. Myocardial infarction was induced in rats by 45 min of ischemia and 120 min of reperfusion. Infarction size and apoptosis were reduced in rats pretreated with angiotensin II type 2 receptor antagonist (AT2-A) or ACE-I, but not by ATI-A. ERK activation and bradykinin-mediated effects were suggested to be the mechanisms of benefits observed in rats treated with AT1-A and ACE-I, respectively.
3. Long-term (5 weeks) effects of ATl-A in hamsters with myocardial infarction was investigated.
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