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Ischemic Neuronal Damade and heat Shock (Stress) Protein

Research Project

Project/Area Number 02670635
Research Category

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

Allocation TypeSingle-year Grants
Research Field Cerebral neurosurgery
Research InstitutionNagoya City University

Principal Investigator

MABE Hideo  Nagoya City University, Department of Neurosurgery, Assistant Professor, 医学部, 助教授 (20093073)

Co-Investigator(Kenkyū-buntansha) KANAI Hideki  Nagoya City University, Department of Neurosurgery, Assistant, 医学部, 助手 (90185893)
NAGAI Hajime  Nagoya City University, Department of Neurosurgery, Professor, 医学部, 教授 (00023747)
Project Period (FY) 1990 – 1991
Project Status Completed (Fiscal Year 1991)
Budget Amount *help
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1991: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1990: ¥1,400,000 (Direct Cost: ¥1,400,000)
KeywordsHeat shock protein 70 / ischemic neuronal damage / Hyperthermia / Ischemic tolerance / Rat
Research Abstract

We investigated the possibility that neuronal cells given a hyperthermic or mild ischemia treatment acquired tolerance to a subsequent, and what would be lethal, ischemic stress in vivo.
Hyperthermia was produced in the rat by placing them in a water bath maintained at 42゚ C. The body temperature of the rat was raised to 42゚ C for 15 min and then the animals were subjected to 15 min of four-vessel occlusion. Seven days after recirculation, the animals were sacrificed, and the brains were removed, fixed in 10% formalin and stained by hematoxylin-eosin for histopathology. In the rat subjected to 15 min of four-vessel occlusion 8 or 24 hours after hyperthermia, ischemic neuronal change in the CA1 was less compared to 15 min of four-vessel occlusion without hyperthermia. The hippocampus from animals subjected to hyperthermia was analysed using immunoblotting. Expression of heat shock proteon 70(HSP 70)was shown in the animals 8 or 24 hours after hyperthermia.
Eight min ischemia 24 hours before 15 min ischemia exhibited protective effect against ischemic neuronal change. Expression of HSP 70 was shown in the hippocampus 24 hours after 8 min ischemia, but was not after 15 min ischemia.
These results provides support for the possibility that hyperthermia or mild ischemia makes the neuronal cells more resistant to the ischemic damage. It is suggested that these tolerance to the ischemic stress correlates to expression of HSP 70.

Report

(3 results)
  • 1991 Annual Research Report   Final Research Report Summary
  • 1990 Annual Research Report
  • Research Products

    (4 results)

All Other

All Publications (4 results)

  • [Publications] H.Mab,A.Umemura H.Kanai,H.Nagai: "The effect of hyperthermea on ischemic nemonal damage" Jonrnal of Cerebral Blood Flow and Metabolism. 11. S′121 (1991)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1991 Final Research Report Summary
  • [Publications] Mabe H, umemura A, Kanai H, Nagai H: "The effect of hyperthermia on ischemic neuronal damage." Journal of Cerebral Blood Flow and Metabolism. 11. S121 (1991)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1991 Final Research Report Summary
  • [Publications] H.Mabe,A.Umemura H.Kanai,H.Nagai: "The effect of hyper thermia on ischemic neuronal demage" Journal of Cerebral Blood Flow and Metabolism. 11. S121 (1991)

    • Related Report
      1991 Annual Research Report
  • [Publications] H.Mabe,A.Umemura,H.kamai,and H.Nagai: "The effect of hyperthermia on ischemic neuronal damage" Journal of Cerebrl Blood Flow and Mefabolism. 11. (1991)

    • Related Report
      1990 Annual Research Report

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Published: 1990-04-01   Modified: 2016-04-21  

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