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

Abstract

The effects of the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME) and the NO donor sodium nitroprusside (SNP) on whole body O2 consumption (V˙o 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˙o 2and systemic vascular resistance (SVR). Data were obtained in each dog under the following conditions: 1) Control 1, 2) SNP (30 μg ⋅ kg−1 ⋅ min−1iv) 3) Control 2, 4)l-NAME (10 mg/kg iv), and 5) SNP and adenosine (30 and 600 μg ⋅ kg−1 ⋅ min−1iv, 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 changedV˙o 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 O2 difference. Both SNP and adenosine returned CO to pre-l-NAME values, butV˙o 2 was unaffected. We conclude that 1) basally released endogenous NO had a tonic systemic vasodilator effect, but it had no influence on V˙o 2; 2) SNP did not alterV˙o 2 before or after inhibition of endogenous NO production; 3) the inability ofl-NAME to increaseV˙o 2 was not because CO, i.e., O2 supply, was reduced below the critical level.