+ Translate

The lung at high altitude: bronchoalveolar lavage in acute mountain sickness and pulmonary edema

, : The lung at high altitude: bronchoalveolar lavage in acute mountain sickness and pulmonary edema. Journal of Applied Physiology 64(6): 2605-2613

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 (.times. 105/ml) in BAL fluid was 3.5 .+-. 2.0 for HAPE, 0.9 .+-. 0.4 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.

(PDF 0-2 workdays service)

Accession: 006712396

PMID: 3403445

Submit PDF Full Text: Here

Submit PDF Full Text

No spam - Every submission is manually reviewed

Due to poor quality, we do not accept files from Researchgate

Submitted PDF Full Texts will always be free for everyone
(We only charge for PDFs that we need to acquire)

Select a PDF file:

Related references

Dehnert, C.; Schneider, M.; Mairbäurl, H.; Bärtsch, P., 2003: Acute mountain sickness and high-altitude pulmonary edema. How to protect the mountain climber from the effects of the "altitude haze". Acute mountain sickness (AMS) usually occurs after 6-12 hours of acute exposure to altitudes above 2,500 m. If there is no further altitude gain, it normally resolves spontaneously within a day or two. However, it may, in rare cases, progress to l...

Cucinell S.A.; Evans W.; Claybaugh J., 1988: Renal differences among acute mountain sickness ams high altitude pulmonary edema hape and high altitude retinopathy har. FASEB Journal 2(5): ABSTRACT 5730

Bärtsch, P., 1993: Acute mountain sickness and high altitude pulmonary edema. Deutsche Medizinische Wochenschrift 118(40): 1463-1464

Kedzierewicz, R.; Cabane, D., 2013: Acute mountain sickness and high altitude cerebral and pulmonary edema. Altitude hypoxia is responsible for acute mountain sickness. It can worsen and generate a high altitude cerebral edema, which can be fatal. After reminding the reader clinical and epidemiological facts, this review aims to present new insights of...

Reinhart, W.H.; Kayser, B.; Singh, A.; Waber, U.; Oelz, O.; Bärtsch, P., 1991: Blood rheology in acute mountain sickness and high-altitude pulmonary edema. The role of blood rheology in the pathogenesis of acute mountain sickness and high-altitude pulmonary edema was investigated. Twenty-three volunteers, 12 with a history of high-altitude pulmonary edema, were studied at low altitude (490 m) and at...

Grissom, C.K.; Zimmerman, G.A.; Whatley, R.E., 1997: Endothelial selectins in acute mountain sickness and high-altitude pulmonary edema. Study objectives: Mechanical or inflammatory injury to pulmonary endothelial cells may cause impaired pulmonary gas exchange in acute mountain sickness (AMS) and noncardiogenic pulmonary edema in high-altitude pulmonary edema (HAPE). This study wa...

Sikri, G.; Bhattacharya, A., 2016: Novel drugs in the management of acute mountain sickness and high altitude pulmonary edema. Open Access Journal of Sports Medicine 7: 1-3

Sutton J.R.; Lassen N., 1979: Patho physiology of acute mountain sickness and high altitude pulmonary edema hypothesis. Human acute mountain sickness (AMS) and high altitude pulmonary edema (HAPO) occur together more often than is realized. It is hypothesized AMS and HAPO have a common pathophysiological basis: both are due to increased pressure and flow in the mic...

Yamaguchi, S.; Kubo, K.; Takabayashi, Y.; Hanaoka, M.; Hayano, T.; Koizumi, T.; Fujimoto, K.; Kobayashi, T., 1996: Cytokines in bronchoalveolar lavage fluid in patients with high-altitude pulmonary edema. European Journal of Clinical Investigation 26(SUPPL 1): A58

Koyama, S.; Kubo, K.; Takabayashi, Y.; Miyahara, T.; Kawashima, A.; Fujimoto, K.; Honda, T.; Matsuzawa, Y.; Kobayashi, T.; Sekiguchi, M., 1993: Analysis of bronchoalveolar lavage fluid in a case of high altitude pulmonary edema. A 29-year-old male climber developed high altitude pulmonary edema (HAPE), progressing from headache and dyspnea to disturbance of consciousness in the Japan Alps. He was admitted to Shinshu University Hospital. Physical examination on admission r...