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Journal of Endotoxin Research
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Bacterial lipopolysaccharide-induced hyporeactivity in perfused rat resistance vessels: modulating effects of dexamethasone

M. Serio

Institute of Medical Pharmacology, University of Bari, Bari, Italy

M.A. Potenza

Institute of Medical Pharmacology, University of Bari, Bari, Italy

M. Montagnani

Institute of Medical Pharmacology, University of Bari, Bari, Italy

G. Mansi

Institute of Medical Pharmacology, University of Bari, Bari, Italy

R. Rinaldi

Institute of Medical Pharmacology, University of Bari, Bari, Italy

S. Pece

Institute of Medical Microbiology, University of Bari, Bari, Italy

D. Fumarola

Institute of Medical Microbiology, University of Bari, Bari, Italy

E. Jirillo

Institute of Medical Microbiology, University of Bari, Bari, Italy

D. Mitolo-Chieppa

Institute of Medical Pharmacology, University of Bari, Bari, Italy

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.

Journal of Endotoxin Research, Vol. 3, No. 6, 491-496 (1996)
DOI: 10.1177/096805199600300607
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