High-altitude pulmonary edema (HAPE), a severe form of altitude illness that can occur in young healthy individuals, is a noncardiogenic form of edema that is associated with high concentrations of proteins and cells in bronchoalveolar lavage (BAL) fluid (Schoene et al., J. Am. Med. Assoc. 256: 63-69, 1986). We hypothesized that acute mountain sickness (AMS) in which gas exchange is impaired to a milder degree is a precursor to HAPE. We therefore performed BAL with 0.89% NaCl by fiberoptic bronchoscopy in eight subjects at 4,400 m (barometric pressure = 440 Torr) on Mt. McKinley to evaluate the cellular and biochemical responses of the lung at high altitude. The subjects included one healthy control (arterial O2 saturation = 83%), three climbers with HAPE (mean arterial O2 saturation = 55.0 ± 5.0%), and four with AMS (arterial O2 saturation = 70.0 ± 2.4%). Cell counts and differentials were done immediately on the BAL fluid, and the remainder was frozen for protein and biochemical analysis to be performed later. The results of this and of the earlier study mentioned above showed that the total leukocyte count (x 105/ml) in BAL fluid was 3.5 ± 2.0 for HAPE, 0.9 ± 4.0 for AMS, and 0.7 ± 0.6 for controls, with predominantly alveolar macrophages in HAPE. The total protein concentration (mg/dl) was 616.0 ± 3.3 for HAPE, 10.4 ± 8.3 for AMS, and 12.0 ± 3.4 for controls, with both large- (immunoglobulin M) and small- (albumin) molecular-weight proteins present in HAPE. There was evidence of complement activation (C5a) and release of thromboxane B2 and leukotriene B4 in HAPE but not in controls or AMS. Despite gas exchange impairment in AMS, the BAL fluid showed no evidence of abnormal protein or cell concentrations.
All Science Journal Classification (ASJC) codes
- Physiology (medical)