INHALATION OF NASALLY DERIVED NITRIC-OXIDE MODULATES PULMONARY-FUNCTION IN HUMANS

The vasodilator gas nitric oxide (NO) is produced in the paranasal sin uses and is excreted continuously into the nasal airways of humans. Th is NO will normally reach the lungs with inspiration. especially durin g nasal breathing. We wanted to investigate the possible effects of lo w-dose inhalation of NO from the nasal airways on pulmonary function. The effects of nasal and oral breathing on transcutaneous oxygen tensi on (tcPo(2)) were studied in healthy subjects. Furthermore. we also in vestigated whether restoring low-dose NO inhalation would influence pu lmonary vascular resistance index (PVRI) and arterial oxygenation (Pao (2)) in intubated patients who are deprived of NO produced in the nasa l airways. Thus. air derived from the patient's own nose was aspirated and led into the inhalation limb of the ventilator. In six out of eig ht healthy subjects tcPo(2) was 10% higher during periods of nasal bre athing when compared with periods of oral breathing. In six out of six long-term intubated patients Pao(2) increased by 18% in response to t he addition of nasal air samples. PVRI was reduced by 11% in four of 1 2 short-term intubated patients when nasal air was added to the inhale d air. The present study demonstrates that tcPo(2) increases during na sal breathing compared with oral breathing in healthy subjects. Furthe rmore. in intubated patients. who are deprived of self-inhalation of e ndogenous NO. Pao(2) increases and pulmonary vascular resistance may d ecrease by adding NO-containing air. derived from the patient's own no se. to the inspired air. The involvement of self-inhaled NO in the reg ulation of pulmonary function may represent a novel physiological prin ciple, namely that of an enzymatically produced airborne messenger. Fu rthermore. our findings may help to explain one biological role of the human paranasal sinuses.