© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Nitric oxide contributes to the regulation of vasomotor tone but does not modulate O2-consumption in exercising swine
Experimental Cardiology, Thoraxcenter, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
* Corresponding author. Tel.: +31-10-408-8029; fax: +31-10-408-9494 duncker{at}tch.fgg.eur.nl
Objective: The role of nitric oxide (NO) in the regulation of vasomotor tone and tissue O2-consumption is incompletely understood. We therefore determined the contribution of endogenous NO to regulation of systemic, pulmonary and coronary vasomotor tone and myocardial (MVO2) and whole body (BVO2) O2-consumption in exercising swine. Methods and results: Exercise (1–5 km/h) up to 85% of maximum heart rate in 11 swine produced a 4-fold increase in BVO2, which was accommodated for by 2-fold increases in both cardiac output (CO) and body O2-extraction. The NO synthase inhibitor N
-nitro-L-arginine (NLA, 20 mg/kg, i.v.) increased mean aortic pressure by 30 mmHg both at rest and during exercise, due to a decrease in systemic vascular conductance from 37±2 to 22±1 ml/min mmHg–1 at rest and from 88±3 to 60±3 ml/min mmHg–1 at 5 km/h (all P
0.05 versus control). NLA produced vasoconstriction at rest and at 5 km/h in virtually all regional beds but did not affect the exercise-induced redistribution of CO. NLA increased mean pulmonary artery pressure from 15±1 to 21±1 mmHg at rest and from 30±2 to 40±2 mmHg at 5 km/h, due to a decrease in pulmonary vascular conductance (all P0.05). BVO2 remained unchanged and consequently the decrease in CO resulted in a compensatory increase in O2-extraction. NLA in a dose of 40 mg/kg produced similar responses. NLA had no significant effect on myocardial O2-demand or MVO2 either at rest or during exercise, but decreased coronary vascular conductance which resulted in a decrease in coronary venous PO2 from 24.5±1.1 to 21.9±0.8 mmHg at rest and from 23.5±0.5 to 21.0±0.6 mmHg at 5 km/h (all P0.05). Conclusions: Endogenous NO dilates the systemic, pulmonary and coronary vascular bed, but does not modify MVO2 or BVO2 in swine at rest and during exercise.
KEYWORDS Coronary circulation; Nitric oxide; Oxygen consumption; Pulmonary circulation; Vasoconstriction/dilation
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