Omura A, Roy R, Jennings T
Albany Medical Center, Dept of Anesthesiology, USA.
Wilderness Environ Med. 2000 Winter;11(4):251-6. doi: 10.1580/1080-6032(2000)011[0251:inoisi]2.3.co;2.
High-altitude pulmonary edema (HAPE) afflicts certain individuals after a rapid gain in elevation. Those susceptible demonstrate an exaggerated hypoxic pulmonary vasoconstrictive response. This causes pulmonary hypertension, which may disrupt vascular integrity. This experiment was designed to test whether inhaled nitric oxide would affect development of HAPE in a rat model.
Subjects were exposed in a hypobaric chamber to a simulated altitude of 6200 m (barometric pressure = 380 mm Hg, fraction of inspired oxygen = 0.19) for 24 hours. Control animals (n = 48) spontaneously breathed a mixture of 90% room air and 10% nitrogen, whereas the nitric oxide group (n = 48) received a similar mixture containing 83 ppm nitric oxide. Postmortem examination of lungs was performed for light microscopy, total hemoglobin, and gravimetric estimates of water content.
Mortality was 39.5% (n = 19) in control animals and 6.2% (n = 3) in the nitric oxide group (P < .001). Both groups significantly increased their lung weight-body weight ratio. Percentage of lung water was similar in both groups despite increases in lung weight, which is consistent with the protein-rich edema characteristic of HAPE. Light microscopic examination of survivors' lungs in both groups revealed scattered alveolar hemorrhage. No significant cellular inflammatory response was present.
We conclude that inhaled nitric oxide improves survival in the rat model of HAPE.
