INHALED NITRIC-OXIDE SELECTIVELY DECREASES PULMONARY VASCULAR-RESISTANCE WITHOUT IMPAIRING OXYGENATION DURING ONE-LUNG VENTILATION IN PATIENTS UNDERGOING CARDIAC-SURGERY

Background: Inhaled nitric oxide (NO), an endothelium-derived relaxing factor, is a selective pulmonary vasodilator. The authors investigate d whether inhaled NO decreases pulmonary vascular resistance (PVR) whi le preserving hypoxic pulmonary vasoconstriction and whether it mainta ins or improves oxygenation in patients during one-lung ventilation. M ethods: In supine cardiac surgical patients with a normal mean pulmona ry artery pressure (PAP) (<25 mmHg, n=10) or a moderately elevated PAP (25-35 mmHg, n=10), one-lung ventilation was established with 80% oxy gen and 20% nitrogen followed by the same gas mixture containing 20 pp m NO for 6 min. Results: Inhaled NO decreased (P<0.05) PAP from 30+/-2 to 27+/-2 mmHg in the patients with moderate pulmonary hypertension. Likewise, PVR decreased (P<0.05) from 266+/-10 to 205+/-8 dyn.s.cm(-5) . The PAP and PVR did not change significantly after NO inhalation in the patients without pulmonary hypertension. All other hemodynamic var iables remained unchanged after inhalation of NO in both groups. In th e patients with pulmonary hypertension, the PAP and PVR returned to ba seline after discontinuation of inhaled NO. Inhaled NO did not signifi cantly change the arterial oxygen tension or venous admixture in eithe r group of patients. Ventilation, airway pressure, tidal volume, and l ung compliance also were unaffected by inhaled NO. Conclusions: This s tudy demonstrates that 20 ppm inhaled NO is a selective pulmonary vaso dilator in patients with moderate pulmonary hypertension secondary to cardiac disease who are undergoing one-lung ventilation. In contrast t o what would be expected with intravenous vasodilators that inhibit hy poxic pulmonary vasoconstriction, inhaled NO does not increase the ven ous admixture or impair oxygenation.