Effect of Nitric Oxide on β-Glucan/Indomethacin-Induced Septic Shock

DOI Web Site Web Site PubMed 被引用文献4件 参考文献53件
  • Nameda Sachiko
    Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science
  • Saito Maki
    Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science
  • Miura Noriko N.
    Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science
  • Adachi Yoshiyuki
    Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science
  • Ohno Naohito
    Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science

書誌事項

タイトル別名
  • Effect of Nitric Oxide on .BETA.-Glucan/Indomethacin-Induced Septic Shock
  • Effect of Nitric Oxide on ベータ Glucan Indomethacin Induced Septic Shock

この論文をさがす

抄録

We have previously shown that repeated administration of nonsteroidal anti-inflammatory drugs (NSAIDs) to mice treated with β-glucan, a biological response modifier, induced severe lethality. The lethality would be strongly related to the translocation of enterobacterial flora to the peritoneal cavity and disruption of the cytokine network. Reports suggest that nitric oxide (NO) can have an effective or detrimental role in septic shock. In the present study, we examined the effect of NO, an inflammatory mediator, on β-glucan/indomethacin (IND)- induced septic shock by inhibiting its synthesis with NG-nitro-L-arginine methyl ester (L-NAME), a nonselective NO synthase (NOS) inhibitor. Nitrite concentration was used as an indicator of NO generation. Mortality in β-glucan/IND-treated mice was increased by administering L-NAME. Numbers of bacteria in various organs of mice treated with β-glucan/IND rose significantly within a couple of days of the administration of L-NAME. Additionally, TNF-α, IL-1β, and IL-6 concentrations were enhanced in peritoneal exuded cells in culture. These results suggest a significant loss of the bactericidal activity of macrophages on the administration of a NOS inhibitor which enhanced the rate of enterobacterial invasion to the peritoneal cavity, resulting in systemic inflammatory response syndrome. The production of NO, therefore, provides a protective effect in β-glucan/IND-induced sepsis.

収録刊行物

被引用文献 (4)*注記

もっと見る

参考文献 (53)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ