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Study on the cardiotoxic actions of botulinolysin and other bacterial thiol-activated hemolysins.

Research Project

Project/Area Number 06670292
Research Category

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

Allocation TypeSingle-year Grants
Research Field Bacteriology (including Mycology)
Research InstitutionOsaka University

Principal Investigator

SUGIMOTO Nakaba  Osaka University, Research Institute for Microbial Diseases, Division of Infectious Diseases, Department of Bacterial Toxinology, Associate Professor, 微生物病研究所, 助教授 (20142317)

Project Period (FY) 1994 – 1995
Project Status Completed (Fiscal Year 1995)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
Keywordsbacterial toxin / Thiol-activated hemolysin / Vascular contractility / Endothelial cells / NO / EDRF / ウエルシュ菌 / θ毒素 / ボツリヌス菌
Research Abstract

(1) Cardiotoxic action of bacterial thiol-activated hemolysins, rheta-toxin (PLO) of Clostridium perfringens and botulinolysin (BL) of Clostridium botulinum, was investigated by using whole rats, and isolated thier orgains and tissues.
(2) Blood pressure of rats abruptly dropped immediately after the i.v.injection of BL.
(3) Ex vivo perfusion of BL and PLO to isolated hearts caused irreversible increase in coronary perfusion pressure and cessation of spontaneous heart beat.
(4) Increase of perfusion pressure by BL was also observed in lungs, livers, or kidneys.
(5) Treatment with BL or PLO increased contractile tension of isolated aortic rings elicited by phenylephrine, alpha-agonist.
(6) Tension elicited by phenylephrine in endothelium-denuded rings was not affected by the treatment with BL or PLO.
(7) Relaxation of the rings by acetylcholine was inhibited concentration-dependently by BL or PLO.
(8) Biochemical confirmation of the actions of BL and PLO on release of EDRF from endothelium was proved to be impossible at the moment because the concentration of NO in perfusate from hearts before and after the perfusion of BL or PLO was too low to be quantified by fluorescent measurement using 2,3-diaminonaphthalene.

Report

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

    (5 results)

All Other

All Publications (5 results)

  • [Publications] Nakaba Sugimoto, et al.: "Coronary vasoconstriction is the most probable cause of cheath of rats intoxicated with botulinolysin, a hemdysin produced by Clostridium botulinum" Toxicon. 33. 1215-1230 (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Nakaba Sugimoto, et al.: "Botulinolysiu, a thiol-activated hemolysin produced by Clostridium bitulinum, inhibits endothelium-dependent relaxation of rat aortic ring." Toxicon. (投稿中).

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Nakaba Sugimoto et al.: "Coronary vsoconstriction is the most probable cause of death of rats intoxicated with botulinolysin, a hemolysin produced by Clostridium botulinum." Toxicon. 33. 1215-1230 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Nakaba Sugimoto et al.: "Botulinolysin, a thiol-activated hemolysin produced by Clostridium botulinum, inhibits endothelium-dependent relaxation of rat aortic ring." Toxicon. submitted.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Nakaba Sugimoto et al.: "Coronary uasoconstriction is the mast prolxrble cause of death of rats intoxicated with bafuluolysin,a hemolysin produced by Clostridain botulinum" Toxicon. 33. 1215-1230 (1995)

    • Related Report
      1995 Annual Research Report

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

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