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The pathophysiology and treatment of postischemic hypoperfusion after complete cerebral ischemia

Research Project

Project/Area Number 63570728
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field 麻酔学
Research InstitutionEhime University

Principal Investigator

ARAI Tatsuru  Ehime University, School of Medicine, Professor, 医学部, 教授 (50033436)

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)
Project Period (FY) 1988 – 1989
Project Status Completed (Fiscal Year 1989)
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)
Keywordsno-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.

Report

(3 results)
  • 1989 Annual Research Report   Final Research Report Summary
  • 1988 Final Research Report Summary
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] 土手健太郎: "虚血後遅発性脳血流減少症の脳循環動態と蘇生後脳機能回復に及ぼす影響-第1編-" 麻酔. 39. (1990)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] 土手健太郎: "虚血後遅発性脳血流減少症の脳循環動態と蘇生後脳機能回復に及ぼす影響-第2編-" 麻酔. 39. (1990)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] Kentaro DOTE: "The effects of post-ischemic delayed hypoperfusion of the process of recovery of brain function" MASUI. 39(3). (1990)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] Kentaro DOTE: "Cerebral hemodynamics of post-ischemic delayed hypoperfusion (PDH) and the effects of Nicardipine of the PDH" MASUI, 39(4), 1990.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] 土手健太郎: "虚血後遅発性脳血流減少症の脳循環動態と蘇生後脳機能回復に及ぼす影響-第1編-" 麻酔. 39. (1990)

    • Related Report
      1989 Annual Research Report
  • [Publications] 土手健太郎: "虚血後遅発性脳血流減少症の脳循環動態と蘇生後脳機能回復に及ぼす影響-第2編-" 麻酔. 39. (1990)

    • Related Report
      1989 Annual Research Report

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Published: 1988-04-01   Modified: 2016-04-21  

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