Lung diffusing capacity for nitric oxide at lowered and raised ambient pressures.

Lung diffusing capacity for NO (DLNO) was determined in eight subjects at ambient pressures of 505, 1015, and 4053hPa (379, 761 and 3040mmHg) as they breathed normoxic gases. Mean values were 116.9±11.1 (SEM), 113.4±11.1 and 99.3±10.1mlmin(-1)hPa(-1)at 505, 1015, and 4053hPa, with a 13% difference between the two higher pressures (P=0.017). The data were applied to a model with two serially coupled conductances; the gas phase (DgNO, variable with pressure), and the alveolo-capillary membrane (DmNO, constant). The data fitted the model well and we conclude that diffusive transport of NO in the peripheral lung is inversely related to gas density. At normal pressure DmNO was approximately 5% larger than DLNO, suggesting that the Dg factor then is not negligible. We also conclude that the density of the breathing gas is likely to impact the backdiffusion of naturally formed NO from conducting airways to the alveoli.

Effects of ambient pressure on pulmonary nitric oxide.

Airway nitric oxide (NO) has been proposed to play a role in the development of high-altitude pulmonary edema. We undertook a study of the effects of acute changes of ambient pressure on exhaled and alveolar NO in the range 0.5-4 atmospheres absolute (ATA, 379-3,040 mmHg) in eight healthy subjects breathing normoxic nitrogen-oxygen mixtures. On the basis of previous work with inhalation of low-density helium-oxygen gas, we expected facilitated backdiffusion and lowered exhaled NO at 0.5 ATA and the opposite at 4 ATA. Instead, the exhaled NO partial pressure (Pe(NO)) did not differ between pressures and averaged 1.21 ± 0.16 (SE) mPa across pressures. As a consequence, exhaled NO fractions varied inversely with pressure. Alveolar estimates of the NO partial pressure differed between pressures and averaged 88 (P = 0.04) and 176 (P = 0.009) percent of control (1 ATA) at 0.5 and 4 ATA, respectively. The airway contribution to exhaled NO was reduced to 79% of control (P = 0.009) at 4 ATA. Our finding of the same Pe(NO) at 0.5 and 1 ATA is at variance with previous findings of a reduced Pe(NO) with inhalation of low-density gas at normal pressure, and this discrepancy may be due to the much longer durations of low-density gas breathing in the present study compared with previous studies with helium-oxygen breathing. The present data are compatible with the notion of an enhanced convective backtransport of NO, compensating for attenuated backdiffusion of NO with increasing pressure. An alternative interpretation is a pressure-induced suppression of NO formation in the airways.

Microgravity decreases and hypergravity increases exhaled nitric oxide.

Inhalation of toxic dust during planetary space missions may cause airway inflammation, which can be monitored with exhaled nitric oxide (NO). Gravity will differ from earth, and we hypothesized that gravity changes would influence exhaled NO by altering lung diffusing capacity and alveolar uptake of NO. Five subjects were studied during microgravity aboard the International Space Station, and 10 subjects were studied during hypergravity in a human centrifuge. Exhaled NO concentrations were measured during flows of 50 (all gravity conditions), 100, 200, and 500 ml/s (hypergravity). During microgravity, exhaled NO fell from a ground control value of 12.3 +/- 4.7 parts/billion (mean +/- SD) to 6.6 +/- 4.4 parts/billion (P = 0.016). In the centrifuge experiments and at the same flow, exhaled NO values were 16.0 +/- 4.3, 19.5 +/- 5.1, and 18.6 +/- 4.7 parts/billion at one, two, and three times normal gravity, where exhaled NO in hypergravity was significantly elevated compared with normal gravity (P