Key result
Patients with chronic heart failure had significantly greater exhaled nitric oxide output during exercise compared to controls (455 vs 152 nl/min/m2, p<0.001), which correlated with impaired oxygen kinetics.
Why the study?
Does exhaled nitric oxide output correlate with impaired oxygen uptake kinetics during exercise in patients with chronic heart failure?
Cross-Sectional (n=23)
No
Does exhaled nitric oxide output correlate with impaired oxygen uptake kinetics during exercise in patients with chronic heart failure?
Absolute Event Rate: 455% vs 152%
p-value: p=<0.001
In patients with chronic heart failure, increased exhaled nitric oxide output during exercise correlates with impaired oxygen uptake kinetics, suggesting a counter-regulatory role in disturbed blood flow.
Exhaled nitric oxide output during exercise was associated with impaired oxygen kinetics in chronic HF; hypothesis-generating and should not yet change practice.
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.
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Funakoshi et al. (1999) conducted a cross-sectional in Chronic Heart Failure (n=23). Chronic Heart Failure vs. Normal controls was evaluated on Exhaled nitric oxide (NO) output during exercise (nl min-1 m-2) (p=<0.001). Patients with chronic heart failure had significantly greater exhaled nitric oxide output during exercise compared to controls (455 vs 152 nl/min/m2, p<0.001), which correlated with impaired oxygen kinetics.
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