| Project/Area Number |
05454272
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
INOUE Michitoshi Osaka University Hospital, Professor, 医学部・付属病院, 教授 (30028401)
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| Co-Investigator(Kenkyū-buntansha) |
KITAKAZE Masafumi Osaka University Hospital, Clinical Fellow, 医学部・付属病院, 医員
KUSUOKA Hideo Osaka University Medical School, Associate Professor, 医学部, 助教授 (00112011)
KUZUYA Tsunehiko Osaka University Medical School, Associate Professor, 医学部, 助教授 (80150340)
HORI Masatsugu Osaka University Medical School, Lecturer, 医学部, 講師 (20124779)
佐藤 洋 大阪大学, 医学部・附属病院, 医員
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,800,000 (Direct Cost: ¥6,800,000)
Fiscal Year 1994: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1993: ¥4,900,000 (Direct Cost: ¥4,900,000)
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| Keywords | adenosine. / ischemic preconditioning. / alpha1-adrenoceptor. / 5'-nucleotidase / 虚血・再潅流障害 / 5'-nucleotidase |
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| Research Abstract |
We have reported that ischemic preconditioning may limit infarct size by increasing 5'-nucleotidase activity. We tested whether alpha1-adrenoceptor stimulation in ischemic preconditioning mediates the infarct size -limiting effect through augmentation of 5'-nucleotidase activity. The coronary artery was occluded four times for 5 min separated by 5 min of reperfusion (ischemic preconditioning) in 82 dogs. Then the coronary artery was occluded for 90 min followed by 6 h of reperfusion. Infarct size normalized by risk area was smaller after ischemic preconditioning that in the control group, even though no difference existed in endomyocardial collateral flow during ischemic. Ectosolic 5'-nucleotidase activity was increased after ischemic preconditioning. However, prazosin blunted the infarct size-limiting effect of ischemic preconditioning. Intermittent alpha1-adrenoceptor stimulation by methoxamine mimicked the increase in 5'-nucleotidase activity and the infarct size-limiting effect, which were abolished by alpha, beta, -methyleneadenosine 5'-diphosphate. Identical results were obtained in the conscious model. Therefore, we conclude that increases in ectosolic 5'-nucleotidase activity due to alpha1-adrenoceptor activation may contribute to the infarct size-limiting effect of ischemic preconditioning.
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