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Am J Physiol Heart Circ Physiol 282: H2278-H2283, 2002; doi:10.1152/ajpheart.00504.2001
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Vol. 282, Issue 6, H2278-H2283, June 2002

Inhibition of NO production increases myocardial blood flow and oxygen consumption in congestive heart failure

Jay H. Traverse, Yingjie Chen, Mingxiao Hou, and Robert J. Bache

Division of Cardiology, Department of Medicine, University of Minnesota Medical School, Minneapolis 55455; and Minneapolis Heart Institute, Abbott Northwestern Hospital, Minneapolis, Minnesota 55407

Coronary blood flow (CBF) and myocardial oxygen consumption (MVO2) are reduced in dogs with pacing-induced congestive heart failure (CHF), which suggests that energy metabolism is downregulated. Because nitric oxide (NO) can inhibit mitochondrial respiration, we examined the effects of NO inhibition on CBF and MVO2 in dogs with CHF. CBF and MVO2 were measured at rest and during treadmill exercise in 10 dogs with CHF produced by rapid ventricular pacing before and after inhibition of NO production with NG-nitro-L-arginine (L-NNA, 10 mg/kg iv). The development of CHF was accompanied by decreases in aortic and left ventricular (LV) systolic pressure and an increase in LV end-diastolic pressure (25 ± 2 mmHg). L-NNA increased MVO2 at rest (from 3.07 ± 0.61 to 4.15 ± 0.80 ml/min) and during exercise; this was accompanied by an increase in CBF at rest (from 31 ± 2 to 40 ± 4 ml/min) and during exercise (both P < 0.05). Although L-NNA significantly increased LV systolic pressure, similar increases in pressure produced by phenylephrine did not increase MVO2. The findings suggest that NO exerts tonic inhibition on respiration in the failing heart.

nitric oxide; synthase; exercise


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