TY - JOUR
T1 - Bacterial lipopolysaccharide-induced hyporeactivity in perfused rat resistance vessels
T2 - Modulating effects of dexamethasone
AU - Serio, M.
AU - Potenza, M. A.
AU - Montagnani, M.
AU - Mansi, G.
AU - Rinaldi, R.
AU - Pece, S.
AU - Fumarola, D.
AU - Jirillo, E.
AU - Mitolo-Chieppa, D.
PY - 1996
Y1 - 1996
N2 - 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.
AB - 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.
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U2 - 10.1177/096805199600300607
DO - 10.1177/096805199600300607
M3 - Article
AN - SCOPUS:79958140454
VL - 3
SP - 491
EP - 496
JO - Innate Immunity
JF - Innate Immunity
SN - 1753-4259
IS - 6
ER -