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- Title
Bacterial lipopolysaccharide-induced hyporeactivity in perfused rat resistance vessels: modulating effects of dexamethasone.
- Authors
Serio, M.; Potenza, M.A.; Montagnani, M.; Mansi, G.; Rinaldi, R.; Pece, S.; Fumarola, D.; Jirillo, E.; Mitolo-Chieppa, D.
- 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.
- Publication
Innate Immunity, 1996, Vol 3, Issue 6, p491
- ISSN
1753-4259
- Publication type
Article
- DOI
10.1177/096805199600300607