Pathogenesis of high-altitude pulmonary oedema

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Pathogenesis of high-altitude pulmonary oedema.

We have read with great interest the paper by WEST et al. [1], regarding the stress failure mechanism of pulmonary capillaries in the pathogenesis of high-altitude pulmonary oedema (HAPE), and would like to add some considerations. HACKETT et al. [2] described a high incidence of HAPE in subjects without the right pulmonary artery. Recently, we have reported a case of unilateral, left sided HAP...

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High altitude-induced pulmonary oedema.

Almost one mountain trekker or climber out of two develops several symptoms of high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. Individual susceptibility is the most important determinant for the occurrence of high altitude pulmonary oedema (HAPE). Symptoms associated with HAPE are incapacitating fatigue, chest tightness, dyspnoea at the slightest effort, or...

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Ultrastructure of high altitude pulmonary oedema.

Heath, D., Moosavi, H., and Smith, P. (1973). Thorax, 28, 694-700. Ultrastructure of high altitude pulmonary oedema. When rats are exposed for 12 hours to simulated high altitude corresponding to the summit of Mount Everest, they develop ultrastructural changes in the lungs. These consist of the formation and protrusion of multiple endothelial vesicles into the pulmonary capillaries. It seems l...

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Pathogenesis of high-altitude pulmonary oedema: direct evidence of stress failure of pulmonary capillaries.

The pathogenesis of high-altitude pulmonary oedema (HAPE) is disputed. Recent reports show a strong correlation between the occurrence of HAPE and pulmonary artery pressure, and it is known that the oedema is of the high-permeability type. We have, therefore, proposed that HAPE is caused by ultrastructural damage to pulmonary capillaries as a result of stress failure of their walls. However, no...

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Haemodynamic studies in high altitude pulmonary oedema.

The clinical and pathological features of acute pulmonary oedema of high altitudes have been the subject of several recent reports (Houston, 1960; Hultgren et al., 1961; Penialoza, 1962; Arias-Stella and Kruger, 1963; Nayak, Roy, and Narayanan, 1964; Menon, 1965; Singh et al., 1965), but the haemodynamic effects of the illness are not well delineated (Fred et al., 1962; Hultgren et al., 1964). ...

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ژورنال

عنوان ژورنال: European Respiratory Journal

سال: 1995

ISSN: 0000-0000,0903-1936

DOI: 10.1183/09031936.95.08111987