Bacterial lipopolysaccharide-induced hyporeactivity in perfused rat resistance vessels: Modulating effects of dexamethasone

M. Serio, M. A. Potenza, M. Montagnani, G. Mansi, R. Rinaldi, S. Pece, D. Fumarola, E. Jirillo, D. Mitolo-Chieppa

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Abstract

The present study was carried out on mesenteric vascular bed from LPS-injected rats in order to investigate possible mechanisms underlying hyporesponsiveness in resistance blood vessels in the course of septic shock syndrome. The involvement of L-arginine (L-Arg)/nitric oxide (NO) pathway was evaluated by administration of L-Arg, which produced a decrease in perfusion pressure in LPS-treated rats, whereas it was ineffective in control rats. Of note, dexamethasone (DEX) pretreatment in endotoxaemic rats significantly reduced the vasorelaxation by L-Arg; however, this non selective inhibitor of inducible-NOS expression was not able to prevent noradrenaline (NA) hyporeactivity. Furthermore, in order to evaluate whether hyporesponsiveness could be due to an altered contraction mechanism, the effect of endothelin (ET)-1 was tested. This peptide was able to markedly enhance the contractile response to noradrenaline in LPS-treated rats. Collectively, our findings suggest that vascular hyporesponsiveness during septic shock can only be partially explained by activation of the L-Arg/NO pathway. Other mechanisms, probably related to smooth muscle cell contractility, may be involved.

Original languageEnglish
Pages (from-to)491-496
Number of pages6
JournalJournal of Endotoxin Research
Volume3
Issue number6
Publication statusPublished - 1996

ASJC Scopus subject areas

  • Immunology
  • Microbiology
  • Toxicology

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    Serio, M., Potenza, M. A., Montagnani, M., Mansi, G., Rinaldi, R., Pece, S., Fumarola, D., Jirillo, E., & Mitolo-Chieppa, D. (1996). Bacterial lipopolysaccharide-induced hyporeactivity in perfused rat resistance vessels: Modulating effects of dexamethasone. Journal of Endotoxin Research, 3(6), 491-496.