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

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Abstract
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 O2consumption (V˙o2) 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˙o2and 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˙o2from 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 O2difference. Both SNP and adenosine returned CO to pre-l-NAME values, butV˙o2was unaffected. We conclude that 1) basally released endogenous NO had a tonic systemic vasodilator effect, but it had no influence on V˙o2; 2) SNP did not alterV˙o2before or after inhibition of endogenous NO production; 3) the inability ofl-NAME to increaseV˙o2was not because CO, i.e., O2supply, was reduced below the critical level.