Nitric oxide does not modulate whole body oxygen consumption in anesthetized dogs

The effects of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and the NO donor sodium nitroprusside (SNP) on whole body O-2 consumption ((V) over doto(2)) were assessed in 16 dogs anesthetized with fentanyl or isoflurane. Cardiac output (CO) and mean arterial pressure (MAP) were measured with standard methods and were used to calculate (V) over doto(2) and systemic vascular resistance (SVR). Data were obtained in each dog under the following conditions: 1) Control 1, 2) SNP (30 mu g.kg(-1).min(-1) iv) 3) Control 2, 4) L-NAME (10 mg/kg iv), and 5) SNP and adenosine (30 and 600 mu g.kg(-1).min(-1) iv, respectively) after L-NAME. SNP reduced MAP by 29 +/- 3% and SVR by 47 +/- 3%, while it increased CO by 39 +/- 9%. L-NAME had opposite effects; it increased MAP and SVR by 24 +/- 4% and 103 +/- 11%, respectively, and it decreased CO by 37 +/- 3%. Neither agent changed (V) over doto(2) from the baseline value of 4.3 +/- 0.2 ml.min(-1).kg(-1), since the changes in CO were offset by changes in the arteriovenous O-2 difference. Both SNP and adenosine returned CO to pre-L-NAME values, but (V) over doto(2) was unaffected. We conclude that 1) basally released endogenous NO had a tonic systemic vasodilator effect, but it had no influence on (V) over doto(2); 2) SNP did not alter (V) over doto(2) before or after inhibition of endogenous NO production; 3) the inability of L-NAME to increase (V) over doto(2) was not because CO, i.e., O-2 supply, was reduced below the critical level.