Nitric oxide controls cardiac substrate utilization in the conscious dog

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Abstract
Objectives: The aim of this study was to determine whether the acute inhibition of nitric oxide (NO) synthase causes changes in cardiac substrate utilization which can be reversed by a NO donor. Methods: NO synthase was blocked by giving 30 mg/kg of nitro-l-arginine (NLA) i.v. to 15 chronically instrumented dogs. Hemodynamics and blood samples from aorta and coronary sinus were taken at control and at 1 and 2 h after NLA. In five dogs, 0.4 mg/kg of the NO donor 3754 was given i.v. 1 h after NLA. In six dogs, angiotensin II was infused over 2 h (20–40 ng/kg/min) to mimic the hemodynamic effects of NLA. Results: Two h after NLA: mean arterial pressure was 153±4 mmHg; MVO2 increased by 38%; cardiac uptake of lactate and glucose increased, respectively, from 20.0±5.0 to 41.0±9.3 μmol/min and from 1.1±0.7 to 6.8±1.5 mg/min (all PP2 increased by 28% and lactate uptake doubled (both PConclusions: The acute inhibition of NO synthase by NLA causes a switch from fatty acids to lactate and glucose utilization by the heart which can be reversed by a NO donor, suggesting an important regulatory action of NO on cardiac metabolism.

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