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J Appl Physiol 86: 1944-1949, 1999;
8750-7587/99 $5.00
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Vol. 86, Issue 6, 1944-1949, June 1999

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

George J. Crystal1,2,3, Xiping Zhou1,2, Ayman A. Halim1, Syed Alam1, Mohammad El-Orbany1, and M. Ramez Salem1,2

1 Department of Anesthesiology, Illinois Masonic Medical Center, Chicago 60657; Departments of 2 Anesthesiology and 3 Physiology and Biophysics, University of Illinois College of Medicine, Chicago, Illinois 60680

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 O2 consumption (VO2) 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 VO2 and systemic vascular resistance (SVR). Data were obtained in each dog under the following conditions: 1) Control 1, 2) SNP (30 µg · kg-1 · min-1 iv) 3) Control 2, 4) L-NAME (10 mg/kg iv), and 5) SNP and adenosine (30 and 600 µg · 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 VO2 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, but VO2 was unaffected. We conclude that 1) basally released endogenous NO had a tonic systemic vasodilator effect, but it had no influence on VO2; 2) SNP did not alter VO2 before or after inhibition of endogenous NO production; 3) the inability of L-NAME to increase VO2 was not because CO, i.e., O2 supply, was reduced below the critical level.

oxygen metabolism; sodium nitroprusside; NG-nitro-L-arginine methyl ester; nitric oxide synthase


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