Inhaled Nitric Oxide Improves Gas Exchange and Lowers Pulmonary Vascular Resistance in Severe Experimental Hyaline Membrane Disease

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Abstract
To determine the effects of inhaled nitric oxide (NO) on pulmonary hemodynamics and gas exchange in experimental hyaline membrane disease (HMD), we studied 16 premature lambs (0.78 term) in two separate protocols. All animals were treated with exogenous surfactant before mechanical ventilation. In protocol 1, we measured the acute response to brief treatment with inhaled NO (20 ppm, 20 min) after 2 h of mechanical ventilation with fraction of inspired oxygen of 1.00 (n = 5). After 2 h, brief NO treatment lowered pulmonary vascular resistance from 0.26 ±0.05 to 0.16 ±0.03 mm Hg- (mL/min)−1 (p < 0.01) and improved gas exchange (arterial Po2, 44 ± 9 mm Hg baseline to 168 ± 45 mm Hg NO, p < 0.01; arterial Pco2 45 ± 5 mm Hg baseline to 35 ± 4 mm Hg NO, p < 0.05). In protocol 2, to determine whether early and continuous treatment with inhaled NO could sustain improvement in gas exchange and pulmonary hemodynamics in severe HMD, we compared the physiologic effects of ventilation with high inspired oxygen concentrations for 3 h with NO (20 ppm, n = 6) and without NO (controls, n = 5). After 3 h, the NO treatment group had sustained reduction in pulmonary vascular resistance (0.10 ± 0.01 mm Hg (mL/ min)−1 NO versus 0.25 ± 0.04 mm Hg (mL/min)−1 control, p < 0.05), increased left pulmonary artery blood flow (204 ± 24 mL/min NO versus 109 ± 15 mL/min control, p < 0.05), and increased arterial Po2 (114 ± 27 mm Hg NO versus 36 ± 11 mm Hg control, p < 0.05). We conclude that inhaled NO causes marked and sustained improvement in pulmonary hemodynamics and gas exchange in severe experimental HMD. We speculate that pulmonary vasoconstriction and ventilation/perfusion abnormalities contribute to the pathophysiology of severe respiratory failure in preterm newborns, and early treatment with inhaled NO may be effective in clinical management of selected premature patients with HMD.

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