The pathophysiology and treatment of postischemic hypoperfusion after complete cerebral ischemia
Project/Area Number |
63570728
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
麻酔学
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Research Institution | Ehime University |
Principal Investigator |
ARAI Tatsuru Ehime University, School of Medicine, Professor, 医学部, 教授 (50033436)
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Co-Investigator(Kenkyū-buntansha) |
TABO Etsuo Ehime University, School of Medicine, Clinical Assistant, 医学部, 助手 (00179871)
高石 和 愛媛大学, 医学部附属病院, 助手 (70179406)
天川 和彦 愛媛大学, 医学部附属病院, 助手 (50136313)
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Project Period (FY) |
1988 – 1989
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Project Status |
Completed (Fiscal Year 1989)
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Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1989: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1988: ¥1,600,000 (Direct Cost: ¥1,600,000)
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Keywords | no-reflow phenomenon / postischemic delayed hypoperfusion / Nicardipine / complete cerebral ischemia / no-eflow現象 |
Research Abstract |
We studied the influences of no-reflow phenomenon and postischemic delayed hypoperfusion (PDH) on recovery of brain functions after transient complete cerebral ischemia using dogs. Cerebral ischemia was produced by clamping of ascending aorta with aorto-atrial bypass formation. No-reflow phenomenon: 100-200 ml of colloidal carbon was injected through aortic arch with 100 mmHg-pressure clamping ascending and descending aorta. The ratio of no-reflow was calculated by measuring the area of colloidal carbon staining on surfaces of coronary section of brain. The formation of no-reflow phenomenon was observed after 15 min of ischemia. Dilution of blood of the brain by physiological saline immediately after aortic clamping resulted in decrease in the no-reflow area. Three min after start of recirculation it was 10% of the surface of coronary section in the dilution group, but more than 70% in the control. After 5 min it was less than 10% in both groups. The brain functions were better in dilution group after 24-48 h. The efficacy of dilution was demonstrated also in histological examination of hippocampal CAl pyramidal cells. PDH: After 15 min of ischemia 20-40% decrease in blood flow in both cerebral cortex and brain stem was observed for 6-10 h following postischemic reactive hyperemia. The administration of Nicardipine 1 ug/kg/min corrected the PDH resulting in improvement of brain functions. Conclusion: We confirmed that 15 min of complete cerebral ischemia brings about both no-reflow phenomenon and PDH, that both contribute deterioration of brain functions, and that treatment of them results in the improvement of postischemic brain functions.
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Report
(3 results)
Research Products
(6 results)