In a porcine model of endotoxic shock, we evaluated the circulatoryand respiratoryeffects of NO synthase (NOS) blockade.Twenty anaesthetised pigs were divided into three groups and studied for 240min after induction of endotoxic shock with lipopolysaccharides of Escherichia coli (LPS). After180min of endotoxic shock, one group (n = 6) received aminoguanidine, another group (n=6) received NG-nitro-L-argininemethyl ester (L-NAME) and a third group (n = 8) received onlyL PS. A sham group (n = 3) was also studied. LPS decreased systemic arterial pressure and cardiac output (CO) and increased mean pulmonary arterial pressure (MPAP), pulmonary vascular resistance (PVR) and heart rate.Significant changes were also observed in compliance (-18.4%) and resistance (+33.6%) of the respiratory system. Aminoguanidine did not modify LPS-dependent effects, while, after L-NAME, a significant increase in MPAP,PVR and SVR and a decrease in CO were observed. In conclusion, aminoguanidine does not play a significant cardiocirculatory and pulmonary role in the short-term dysfunction of endotoxic shock, while L-NAME has a detrimental effect on haemodynamics, suggesting a protective role of constitutive NOproduction at vascular level during the early stages of endotoxaemia. 2002 Elsevier Science Ltd.All rights reserved.
Effect of NO synthase inhibition on cardiovascular and pulmonary disfunction in a porcine short-term model of endotoxic shock
Lafortuna CL;
2002
Abstract
In a porcine model of endotoxic shock, we evaluated the circulatoryand respiratoryeffects of NO synthase (NOS) blockade.Twenty anaesthetised pigs were divided into three groups and studied for 240min after induction of endotoxic shock with lipopolysaccharides of Escherichia coli (LPS). After180min of endotoxic shock, one group (n = 6) received aminoguanidine, another group (n=6) received NG-nitro-L-argininemethyl ester (L-NAME) and a third group (n = 8) received onlyL PS. A sham group (n = 3) was also studied. LPS decreased systemic arterial pressure and cardiac output (CO) and increased mean pulmonary arterial pressure (MPAP), pulmonary vascular resistance (PVR) and heart rate.Significant changes were also observed in compliance (-18.4%) and resistance (+33.6%) of the respiratory system. Aminoguanidine did not modify LPS-dependent effects, while, after L-NAME, a significant increase in MPAP,PVR and SVR and a decrease in CO were observed. In conclusion, aminoguanidine does not play a significant cardiocirculatory and pulmonary role in the short-term dysfunction of endotoxic shock, while L-NAME has a detrimental effect on haemodynamics, suggesting a protective role of constitutive NOproduction at vascular level during the early stages of endotoxaemia. 2002 Elsevier Science Ltd.All rights reserved.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
