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 (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 O₂ and systemic vascular resistance (SVR). Data were obtained in each dog under the following conditions: 1) Control 1, 2) SNP (30 µg · kg¹ · min¹ iv) 3) Control 2, 4) L-NAME (10 mg/kg iv), and 5) SNP and adenosine (30 and 600 µg · kg¹ · min¹ 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 O₂ from the baseline value of 4.3 ± 0.2 ml · min¹ · kg¹, 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, but O₂ was unaffected. We conclude that 1) basally released endogenous NO had a tonic systemic vasodilator effect, but it had no influence on O₂; 2) SNP did not alter O₂ before or after inhibition of endogenous NO production; 3) the inability of L-NAME to increase O₂ was not because CO, i.e., O₂ supply, was reduced below the critical level.

oxygen metabolism; sodium nitroprusside; N^G-nitro-L-arginine methyl ester; nitric oxide synthase

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