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Am. J. Respir. Crit. Care Med., Volume 163, Number 2, February 2001, 368-373

Hypoxia Decreases Exhaled Nitric Oxide in Mountaineers Susceptible to High-Altitude Pulmonary Edema

THILO BUSCH, PETER BÄRTSCH, DIRK PAPPERT, EKKEHARD GRÜNIG, WULF HILDEBRANDT, HUBERT ELSER, KONRAD J. FALKE, and ERIK R. SWENSON

Department of Anesthesiology and Intensive Care Medicine, Charité, Campus Virchow-Klinikum, Humboldt-University, Berlin, Germany; and Departments of Sports Medicine, Cardiology, and Nuclear Medicine, Ruprecht-Karls-University, Heidelberg, Germany

An exaggerated hypoxic pulmonary vasoconstriction is essential for development of high-altitude pulmonary edema (HAPE). We hypothesized that susceptibility to HAPE may be related to decreased production of nitric oxide (NO), an endogenous modulator of pulmonary vascular resistance, and that a decrease in exhaled NO could be detected during hypoxic exposure. Therefore, we investigated respiratory tract NO excretion by chemiluminescence and pulmonary artery systolic pressure (Ppa,s) by echocardiography in nine HAPE-susceptible mountaineers and nine HAPE-resistant control subjects during normoxia and acute hypoxia (fraction of inspired oxygen [FIO2] = 0.12). The subjects performed oral breathing. Nasally excreted NO was separated from respiratory gas by suction via a nasal mask. In HAPE-susceptible subjects, NO excretion in expired gas significantly decreased (p < 0.05) during hypoxia of 2 h in comparison with normoxia (28 ± 4 versus 21 ± 2 nl/min, mean ± SEM). In contrast, the NO excretion rate of control subjects remained unchanged (31 ± 6 versus 33 ± 6 nl/ min, NS). Nasal NO excretion did not differ significantly between groups during normoxia (HAPE-susceptible group, 183 ± 16 nl/ min; control subjects, 297 ± 55 nl/min, NS) and was not influenced by hypoxia. The changes in Ppa,s with hypoxia correlated with the percent changes in lower respiratory tract NO excretion (R = -0.49, p = 0.04). Our data provide the first evidence of decreased pulmonary NO production in HAPE-susceptible subjects during acute hypoxia that may contribute among other factors to their enhanced hypoxic pulmonary vascular response.




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