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 language | English |
|---|---|
| Pages (from-to) | 491-496 |
| Number of pages | 6 |
| Journal | Innate Immunity |
| Volume | 3 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 1996 |
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ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
- Immunology
- Microbiology
- Infectious Diseases
Cite this
Bacterial lipopolysaccharide-induced hyporeactivity in perfused rat resistance vessels : Modulating effects of dexamethasone. / Serio, M.; Potenza, M. A.; Montagnani, M.; Mansi, G.; Rinaldi, R.; Pece, S.; Fumarola, D.; Jirillo, E.; Mitolo-Chieppa, D.
In: Innate Immunity, Vol. 3, No. 6, 1996, p. 491-496.Research output: Contribution to journal › Article
}
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.
UR - http://www.scopus.com/inward/record.url?scp=79958140454&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79958140454&partnerID=8YFLogxK
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 -