Increased exhaled nitric oxide and impaired oxygen uptake (VO2) kinetics during exercise in patients with chronic heart failure

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 ((V) over dot O-2) 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 (V) over dot O-2 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 mi, p<0.01) and the time constant for (V) over dot O-2 increment was also significantly prolonged in the CHF group (35.1+/-8.0s 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 (V) over dot O-2 increment (r=0.74, p<0.001). Increased NO output played a counter-regulatory role in the impaired blood flow in CHF.