Effects of nitric oxide on blood flow distribution and O2 extraction capabilities during endotoxic shock

Abstract

Zhang, Haibo, Peter Rogiers, Nadia Smail, Ana Cabral, Jean-Charles Preiser, Marie-Odile Peny, and Jean-Louis Vincent.Effects of nitric oxide on blood flow distribution and O2 extraction capabilities during endotoxic shock. J. Appl. Physiol.83(4): 1164–1173, 1997.—The effects of the nitric oxide (NO) synthase inhibitor N G-monomethyl-l-arginine (l-NMMA) and the NO donor 3-morpholinosydnonimine (SIN-1) were tested in 18 endotoxic dogs. l-NMMA infusion (10 mg ⋅ kg−1 ⋅ h−1) increased arterial and pulmonary artery pressures and systemic and pulmonary vascular resistances but decreased cardiac index, left ventricular stroke work index, and blood flow to the hepatic, portal, mesenteric, and renal beds. SIN-1 infusion (2 μg ⋅ kg−1 ⋅ min−1) increased cardiac index; left ventricular stroke work index; and hepatic, portal, and mesenteric blood flow. It did not significantly influence arterial and pulmonary artery pressures but decreased renal blood flow. The critical O2delivery was similar in thel-NMMA group and in the control group (13.3 ± 1.6 vs. 12.8 ± 3.3 ml ⋅ kg−1 ⋅ min−1) but lower in the SIN-1 group (9.1 ± 1.8 ml ⋅ kg−1 ⋅ min−1, both P < 0.05). The critical O2 extraction ratio was also higher in the SIN-1 group than in the other groups (58.7 ± 10.6 vs. 42.2 ± 7.6% in controls, P < 0.05; 43.0 ± 15.5% inl-NMMA group, P = not significant). We conclude that NO is not implicated in the alterations in O2 extraction capabilities observed early after endotoxin administration.