In twelve anaesthetised, mechanically ventilated pigs we evaluated the role of nitric oxide (NO) in cardiovascular dysfunction during endotoxic shock obtained by infusion of E. coli lipopoly saccharides (LPS, 20 microg/kg/h). NG-nitro-L-arginine methyl ester (L-NAME), a non selective inhibitor of NO synthases, was i.v. administered in six animals (control group) to evaluate the basal release of NO and in other six pigs (LPS group) to evaluate the involvement of NO on cardiovascular dysfunction during acute phase of endotoxic shock. Results showed that the cardiovascular changes caused by L-NAME did not differ between groups. This reveals that in pigs, during the acute phase of endotoxic shock there is not an enhanced release of NO. Furthermore, the marked cardiac dysfunction, essentially evidenced by the decrease in stroke volume observed during endotoxic shock, is not NO-dependent. Hence, we suggest that the basal release of this mediator, ensuring an adequate coronary perfusion, exerts a protective role on cardiac activity.

Endotoxic shock and cardiac dysfunction: role of nitric oxide / M. Albertini, S. Mazzola, M.G. Clement. - In: BIOMEDICAL RESEARCH. - ISSN 0970-938X. - 11:1(2000), pp. 19-26.

Endotoxic shock and cardiac dysfunction: role of nitric oxide

M. Albertini
Primo
;
S. Mazzola
Secondo
;
M.G. Clement
Ultimo
2000

Abstract

In twelve anaesthetised, mechanically ventilated pigs we evaluated the role of nitric oxide (NO) in cardiovascular dysfunction during endotoxic shock obtained by infusion of E. coli lipopoly saccharides (LPS, 20 microg/kg/h). NG-nitro-L-arginine methyl ester (L-NAME), a non selective inhibitor of NO synthases, was i.v. administered in six animals (control group) to evaluate the basal release of NO and in other six pigs (LPS group) to evaluate the involvement of NO on cardiovascular dysfunction during acute phase of endotoxic shock. Results showed that the cardiovascular changes caused by L-NAME did not differ between groups. This reveals that in pigs, during the acute phase of endotoxic shock there is not an enhanced release of NO. Furthermore, the marked cardiac dysfunction, essentially evidenced by the decrease in stroke volume observed during endotoxic shock, is not NO-dependent. Hence, we suggest that the basal release of this mediator, ensuring an adequate coronary perfusion, exerts a protective role on cardiac activity.
pig ; endotoxic shock ; nitric oxide ; cardiac dysfunction
Settore VET/02 - Fisiologia Veterinaria
http://www.biomedres.org
Article (author)
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

Caricamento pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/187328
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact