Endotoxic shock and cardiac dysfunction: role of nitric oxide

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.