Increased Exhaled Nitric Oxide and Impaired Oxygen Uptake (VO₂) Kinetics During Exercise in Patients With Chronic Heart Failure

Abstract

Vascular endothelial function is abnormal in patients with congestive heart failure (CHF). Exhaled nitric oxide (NO) output is a marker of pulmonary endothelial NO release. The present study examined the relation between exhaled NO output and oxygen uptake (VO₂) kinetics at the onset of exercise, which reflects blood flow response. Sixteen patients with CHF and 7 volunteers underwent constant bicycle exercise. Oxygen deficit and time constant for VO₂ increment at the onset of exercise were analyzed. Exhaled NO concentration was measured by a chemiluminescence analyzer and exhaled NO output was calculated by multiplexing ventilation. Exhaled NO output was significantly greater in the CHF group than in the control group at rest (86±65 nl min^-1 m ^-2 vs 298±135 nl min^-1 m ^-2, p<0.001) and during exercise (152±98 nl min^-1 m^-2 vs 455±190 nl min^-1 m^-2, p<0.001). However, the %increase of NO output was significantly smaller in the CHF group than in the control group (70±26% vs 109±85%, p<0.05). Oxygen deficit was significantly greater in the CHF group than in the control group (240±70 ml vs 372 ±107 ml, p<0.01) and the time constant for VO₂ increment was also significantly prolonged in the CHF group (35.1±8.0 s vs 50.1±16.3 s, p<0.05). Exhaled NO output during exercise significantly correlated with oxygen deficit (r=0.67, p<0.001) and the time constant for VO₂ increment (r=0.74, p<0.001). Increased NO output played a counter-regulatory role in the impaired blood flow in CHF. (Jpn Circ J 1999; 63: 255 - 260)