Exhaled nitric oxide and pulmonary artery pressures during graded ascent to high altitude

Abstract

Nitric oxide (NO) is a potent vasodilator that regulates pulmonary vascular tone. During ascent to high altitude, pulmonary vascular tone increases leading to pulmonary hypertension. To explore the mechanisms underpinning this effect, we investigated the relationship between exhaled NO (P(E(NO)); nm Hg) and pulmonary artery systolic pressure (PASP; mm Hg) in 11 healthy adults during hypoxic challenge at sea level [with oxygen saturations (S(P(O(2)))) of 80% and 90%] and at intervals during graded ascent to 5050 m. During normobaric hypoxia, PASP progressively increased from 22.7 mm Hg to 33.5 mm Hg (p=0.006), whilst P(E(NO)) remained unchanged. In contrast, during ascent to high altitude, PASP increased progressively from 22.7 mm Hg to 39.1 mm Hg (p<0.001), but P(E(NO)) decreased from 18.8 nm Hg to 9.0 nm Hg (p<0.001). However, after appropriate adjustments, P(E(NO)) had no significant effect on PASP at altitude (p=0.309). These findings indicate that although exhaled NO decreases with altitude, it does not appear to be a major contributor to hypoxic pulmonary vasoconstriction.