Inhaled nitric oxide selectively decreases pulmonary vascular resistance without impairing oxygenation during one-lung ventilation in patients undergoing cardiac surgery

• Published in: Anesthesiology (Philadelphia) 1994, Vol.80 (1), p.57-62
• Main Authors: RICH, G. F, LOWSON, S. M, JOHNS, R. A, DAUGHERTY, M. O, UNCLES, D. R
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Cardiac Surgical Procedures; Cardiovascular system; Humans; Lung - drug effects; Lung - physiology; Medical sciences; Middle Aged; Nitric Oxide - pharmacology; Oxygen Consumption - physiology; Pharmacology. Drug treatments; Respiration, Artificial; Vascular Resistance - drug effects; Vascular Resistance - physiology; Vasodilator agents. Cerebral vasodilators
• ISSN: 0003-3022; 1528-1175
• DOI: 10.1097/00000542-199401000-00012

Inhaled nitric oxide (NO), an endothelium-derived relaxing factor, is a selective pulmonary vasodilator. The authors investigated whether inhaled NO decreases pulmonary vascular resistance (PVR) while preserving hypoxic pulmonary vasoconstriction and whether it maintains or improves oxygenation in patients during one-lung ventilation. In supine cardiac surgical patients with a normal mean pulmonary artery pressure (PAP) (< 25 mmHg, n = 10) or a moderately elevated PAP (25-35 mmHg, n = 10), one-lung ventilation was established with 80% oxygen and 20% nitrogen followed by the same gas mixture containing 20 ppm NO for 6 min. 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 variables remained unchanged after inhalation of NO in both groups. In the patients with pulmonary hypertension, the PAP and PVR returned to baseline after discontinuation of inhaled NO. Inhaled NO did not significantly change the arterial oxygen tension or venous admixture in either group of patients. Ventilation, airway pressure, tidal volume, and lung compliance also were unaffected by inhaled NO. This study demonstrates that 20 ppm inhaled NO is a selective pulmonary vasodilator in patients with moderate pulmonary hypertension secondary to cardiac disease who are undergoing one-lung ventilation. In contrast to what would be expected with intravenous vasodilators that inhibit hypoxic pulmonary vasoconstriction, inhaled NO does not increase the venous admixture or impair oxygenation.