Inhaled Nitric Oxide (NO) improves gas exchange and lowers pulmonary vascular resistance in experimental HMD. However, the effects of inhaled NO on lung diffusing capacity and lung mechanics in HMD remain unclear. Inhaled NO may oxydize alveolar surfactant or increase vascular lung leak. These phenomenons could alter the mechanical properties and transfer capacity of the lungs. Eighteen moderately premature lambs (130 days gestation, term=147 days) were randomly assigned to treatment with 20 ppm inhaled NO or control. After exogenous surfactant administration (Curosurf® 100 mg/kg), the lambs were mechanically ventilated to maintain PaCO2 values between 40 and 50 mm Hg and SpO2 values between 90 and 95%. Lambs were paralysed with pancuronium. After 5 hours of mechanical ventilation, static lung compliance (Cst) was calculated at 10 ml/kg of tidal volume. Functional residual capacity (FRC), and carbon monoxide diffusing capacity (DLco) were measured by using the“single breath method”. From the end expiratory volume, 15 ml/kg of gas mixture containing 0.1% CO, 12% Helium, and 88% air were inhaled. After 10 s exhaled gas was analysed to calculate FRC and DLCO. DLCO was normalized for FRC, and FRC and Cst were normalized for lambs weight. Static compliance and functional residual capacity were not significantly different in the NO vs. control group. In spite of similar mechanical properties of the lung in both groups, lung diffusing capacity was increased in the NO group. In conclusion, no deleterious effects of short term NO inhalation (5 hours) could be demonstrated on mechanical properties in premature lambs with HMD. Increased lung transfer capacity in the NO group probably results from increased pulmonary blood flow.Table

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