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Inducible nitric oxide synthase and neonatal hypoxic-ischemic encephalopathy

Research Project

Project/Area Number 11671068
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Embryonic/Neonatal medicine
Research InstitutionKYOTO UNIVERSITY

Principal Investigator

HATTORI Haruo  Kyoto University, Graduate School of Medicine, Lecturer, 医学研究科, 講師 (80189571)

Project Period (FY) 1999 – 2000
Project Status Completed (Fiscal Year 2000)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Keywordsneonatal hypoxic-ischemic encephalopathy / nitric oxide / inducible nitric oxide synthase / mRNA
Research Abstract

The neuroprotective effect of a selective inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine, was evaluated in a neonatal hypoxic-ischemic rat model. We also measured the changes in nitric oxide (NO) metabolites in the brain. Unilateral hypoxic-ischemic injury was produced in the brain of 7-day-old rats by combining a common carotid artery ligation with hypoxic exposure (8% oxygen) for 2.5 h. Histological evaluation of the brain damage was performed 72 h later. Brain NO metabolites were measured by using a NO analyzer at 0 h, 1.5 h (during hypoxia), 2.5 h (end of hypoxia), 6 h, 24 h, and 72 h after the start of hypoxia. Aminoguanidine (300 mg/kg) was injected intraperitoneally nine times at eight-hour intervals starting 1 h before the hypoxia. These selective iNOS inhibitor administrations resulted in 89% reduction of both the cerebral cortical and the striatal infarcted areas compared to those of vehicle injected controls. Repeated injections of aminoguanidine also suppressed the peak of NO metabolites in the brain during the reoxygenation period. These results indicate that NO generated by iNOS during reoxygenation plays a key role in producing neonatal hypoxic-ischemic brain damage. Brain mRNA was measured semiquantitatively at 0 h, 1.5 h (during hypoxia), 2.5 h (end of hypoxia), 6 h, 24 h, 72 h and 96 h after the start of hypoxia. In either hemisphere of the brain, mRNA was detected at 72 h and 96 h after the start of hypoxia. The iNOS inhibitor tended to suppress the emergence of the mRNA.

Report

(3 results)
  • 2000 Annual Research Report   Final Research Report Summary
  • 1999 Annual Research Report
  • Research Products

    (5 results)

All Other

All Publications (5 results)

  • [Publications] 辻雅弘: "誘導型一酸化窒素合成酵素(inducible nitric oxide synthase,iNOS)阻害剤による新生児低酸素性虚血性脳症の軽減"Brain Hypoxia. 14. 15-23 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Tsuji M: "The protective effect of aminoguanidine on hypoxic-ischemic brain damage and the temporal profile of brain nitric oxide in a neonatal rat"Pediatric Research. 47. 79-83 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Tsuji M: "The protective effect of aminoguanidine on hypoxic-ischemic brain damage and the temporal profile of brain nitric oxide in a neonatal rat"Pediatric Research. 47. 79-83 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Tsuji M: "The protective effect of aminoguanidine on hyposic-ischemic brain damage and the temporal profile of brain nitric oxide in a neonatal rat"Pediatric Research. 47(1). 79-83 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] Tsuji M: "The protective effect of aminoguanidine on hypoxic-ischemic brain damage and the temporal profile of brain nitric oxide in a neonatal rat"Pediatric Research. 47. 79-83 (2000)

    • Related Report
      1999 Annual Research Report

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Published: 1999-04-01   Modified: 2016-04-21  

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