Pathogenesis of high-altitude pulmonary edema

Authors

  • John B. West University of California, Departments of Medicine and Physiology. San Diego, USA. anda Dartmouth Medical School, Department of Medicine. Hanover, New Hampshire, USA.
  • Gene L. Colice University of California, Departments of Medicine and Physiology. San Diego, USA. anda Dartmouth Medical School, Department of Medicine. Hanover, New Hampshire, USA.
  • Yan-Jie Lee University of California, Departments of Medicine and Physiology. San Diego, USA. anda Dartmouth Medical School, Department of Medicine. Hanover, New Hampshire, USA.
  • Yasuo Namba University of California, Departments of Medicine and Physiology. San Diego, USA. anda Dartmouth Medical School, Department of Medicine. Hanover, New Hampshire, USA.
  • Sanli s. Kurdak Departamento de medicina, Universidad de California y Departamento de medicina y psicología, Dartmouth Medical School
  • Zhenxing Fu University of California, Departments of Medicine and Physiology. San Diego, USA. anda Dartmouth Medical School, Department of Medicine. Hanover, New Hampshire, USA.
  • Lo-Chang Ou University of California, Departments of Medicine and Physiology. San Diego, USA. anda Dartmouth Medical School, Department of Medicine. Hanover, New Hampshire, USA.
  • Odile Mathieu-Costello University of California, Departments of Medicine and Physiology. San Diego, USA. anda Dartmouth Medical School, Department of Medicine. Hanover, New Hampshire, USA.

Keywords:

stress failure of pulmonary capillaries, pulmonary hypertension

Abstract

Madison strain Sprague-Dawlet rats were exposed to low barometric pressures of 2g4 and 236 torr, or 8.5 % oxygen at normal pressure for 8- 10 hours. This resulted in an increase of pulmonary artery or right ventricular  systolic pressure from 30.5  to  49  torr. Ultrastructural studies of the lung showed evidence of stress failure of pulmonary capillaries including disruption of the capillary endothelial layer, alveolar epithelial layer, or all layer of the wall, red blood cells (RBCs) and edema fluid in the alveolar wall interstitium, proteinaceous fluid and RBCS in the alveolar spaces, and fluid-filled protrusions of the endothelium into the capillary lumen. These appearances are consistent with the ultrastructural changes we have previously described in rabbit lung when the capillaries are exposed to high transmural pressures, strongly suggesting that the pathogenesis of  HAPE  is stress failure of pulmonary capillaries. 

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Published

2025-07-17

How to Cite

B. West, J., L. Colice, G., Lee, Y.-J., Namba, Y., s. Kurdak, S., Fu, Z., … Mathieu-Costello, O. (2025). Pathogenesis of high-altitude pulmonary edema. Acta Andina, 4(2), 113–116. Retrieved from https://revistas.upch.edu.pe/index.php/AA/article/view/6061

Issue

Vol. 4 No. 2 (1995): Acta Andina

Section

ARTICULOS

License

Copyright (c) 2024 John B. West, Gene L. Colice, Yan-Jie Lee, Yasuo Namba, Sanli s. Kurdak, Zhenxing Fu, Lo-Chang Ou, Odile Mathieu Costello

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