Nitric oxide is present in high concentration in the human nasal airways. During inspiration through the nose a bolus is transported to the lungs. In a randomized cross-over study the effect of two different patterns of breathing, nasal breathing and mouth breathing, was evaluated in 10 patients (mean age 65 years), breathing room air the morning of the first post-operative day after open heart surgery. Nasal breathing is defined as inspiration through the nose and expiration through the mouth, whilst mouth breathing is the converse of this: inspiration through the mouth and expiration through the nose. Pressure in the pulmonary artery and left atrium or pulmonary artery wedge was measured together with thermodilution cardiac output and arterial and mixed venous oxygenation and acid-base parameters. Pulmonary vascular resistance index (PVRI), venous admixture and alveolar-arterial gradient were calculated. Nasal breathing resulted in a lower PVRI, 256 dyn s cm-5 cm-2 vs. 287 (P < 0.01). The oxygen and carbon dioxide tension and pH of arterial and mixed venous blood, venous admixture and the alveolar-arterial gradient remained unchanged. The decreased level of PVRI during nasal breathing compared to that during mouth breathing supports the notion, that endogenous nitric oxide acts as an airborne messenger to modulate the pulmonary vascular tone during normal breathing.

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Interestingly, pulmonary vascular dysfunction after CPB was accompanied by a reduction in the exhaled nitric oxide response to nitroglycerin and lower levels of basal exhaled nitric oxide. The ACh-induced responses in exhaled nitric oxide were unchanged, which could indicate nitric oxide-independent mechanisms behind the endothelial dysfunction in this study. The possibility of using exhaled nitric oxide dynamics to investigate pulmonary endothelial dysfunction merits further studies.