1987 Fiscal Year Final Research Report Summary
The mechanism of cellular dysfunction after ischemia and reperfusion
| Project/Area Number |
61480328
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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 |
麻酔学
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| Research Institution | Nippon Medical School (1987)
Gunma University (1986) |
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Principal Investigator |
OGAWA Ryo Nippon Medical School Professor, 教授 (20008345)
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| Co-Investigator(Kenkyū-buntansha) |
KUNIMOTO Fumio Gunma University, School of Mediaine, associate, 医学部, 助手 (70125847)
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| Project Period (FY) |
1986 – 1987
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| Keywords | Ischemia and reperfusion / cellular injury / lipoperoxide / ショック.スーパーオキシドデイスムターゼ |
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| Research Abstract |
the present study was undertaken to clarify the mechanism and to develop the preventive measures of cellular dysfunction induced by ischemia and reperfusion. The results are summarized as followed:
(1)The rats with cardiac arrest for 7 min showed an incresed lipoperoxide (LPO) in the brain and disturbed ambulation frequency. Nicardipine and nimodipine given prior to the cardiac arrest showed a protective effect on the CNS against anoxia.
(2)The rats with various types of shock such as hemorrhagic shock, endotoxin shock and splanchnic ischemia shock depicted significant elevations of hepatic LPO concentration, concomittantly with marked increases in Xanthine oxidase (XOD) and significant decreases in Superoxide dismutase (SOD).
(3)The cellular dysfunction was certified in a model in which the lung was placed in an oxygen free radical production system.
(4)The production of oxygen free radicals in the cells was detected by a bioluminescence machine using a lusiferine as a photo-intensifier applied on a tissue homogenates.
(5)The effectiveness of various measures to prevent lipoperoxidation were evaluated in rats with endotoxin shock or splanchnic ischemia shock. A high dose of SOD elevated the survival rate significantly.
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