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Effects of halogenated inhalated anesthetics on nitric oxide (NO) signal transduction system.

Research Project

Project/Area Number 06454452
Research Category

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

Allocation TypeSingle-year Grants
Research Field Anesthesiology/Resuscitation studies
Research InstitutionJikei University

Principal Investigator

MASAKI Eiji  Jikei University School of Medicine, Department of Anesthesiology, Lecture, 医学部, 講師 (40221577)

Co-Investigator(Kenkyū-buntansha) AMAKI Yoshikiyo  Jikei University School of Medicine, Department of Anesthesiology, Professor, 医学部, 教授 (30056767)
MORIYAMA Michiko  Jikei University School of Medicine, Department of Anesthesiology, Assistant, 医学部, 助手 (00246448)
KONDOU Tutomu  Jikei University School of Medicine, Department of Anesthesiology, Assistant, 医学部, 助手 (90211250)
Project Period (FY) 1994 – 1995
Project Status Completed (Fiscal Year 1995)
Budget Amount *help
¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥3,100,000 (Direct Cost: ¥3,100,000)
KeywordsNitric oxide (NO) / Reduced iron / Halogenated volatile anesthetics / Hemeprotein / Neurotransmitter / 一酸化窒素(NO) / 揮発性吸入麻酔薬 / グアニレートサイクレース(GC)
Research Abstract

Nitric Oxide (NO) is unique molecule produced by numerous tissues and cells. In CNS,NO acts as a neurotransmitter and mediates excitatory amino acid-stimulation. It is suggested that those action of NO is associated with expression of memory, consciousness and pain. The receptor for NO is enzyme celled guanylate cyclase (GC) which is a reduced iron-containing hemeprotein, catalyzing the synthesis of cGMP.NO activates GC by binding to the reduced iron. Halogenated inhalate volatile anesthetics is also known to interact with hemeprotein like cytochrome P-450 and hemoglobin through the reduced iron. Although many experiments were done to determine the site of action of inhalate volatile anesthetics, it is still unknown. In addtion, several studies indicate that various agents blocking the excitatory amino acid-NO-cGMP pathway have the anesthetic action. Then, we examine the effects of inhalate volatile anrsthetics on NO-stimulated GC activity in rat brain soluble fraction.
The brain solubl … More e fraction was made from male Spague-Dawley rats. The incubation were initiated by adding brain soluble fraction with NO solution and satulated volatele anesthetics buffer. NO and anesthetic concentration were monitored with NO monitor and gasclomatoglaphy, respectively. GC activity was determined by measuring c-GMP,the final product of NO-signal trunsduction pathway, by enzymeimmunoassay. No stimulated GC activity at the lebel of as low as 2 X 10^<-9>. One of the main volatile anesthetics, halothane (H) dose-dependently (0.5-2.7mM) inhibited NO-stimulated GC activity. Moreover, GC activity was also inhibited by H without NO stimulation in brain soluble fraction. These results suggest that 1) : H and NO compete the site of activation of GC (probably reduced iron), 2) : bisides the competition with NO,H has other sites to inhibit GC activity.
Further investigation should be needed to explain whether these effects of halothane is associated with the site of action of inhalated volatile anesthetics. Less

Report

(3 results)
  • 1995 Annual Research Report   Final Research Report Summary
  • 1994 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] 正木英二ら: "NOとハロセンの脳グアニレートサイクレースにおける相互作用" J Anesthesia. 9. A303- (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Eiji Masaki et al: "interaction of nitric oxide and halothane at rat brain guanylate cyclase." J Anesthesia. 9. A303 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] 正木英二ら: "NOとハロセンの脳グアニレートサイクレースにおける相互作用" J Anesthesia. 9. A303 (1995)

    • Related Report
      1995 Annual Research Report

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Published: 1994-04-01   Modified: 2016-04-21  

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