Evidence against an increase in capillary permeability in subjects exposed to high altitude

• Verfasst von: Kleger, Gian-Reto [VerfasserIn]
• Verfasst von: Bärtsch, Peter [VerfasserIn]
• Verfasst von: Vock, Peter [VerfasserIn]
• Verfasst von: Heilig, Bernhard [VerfasserIn]
• Verfasst von: Roberts, L. Jackson [VerfasserIn]
• Verfasst von: Ballmer, Peter E. [VerfasserIn]
• Titel: Evidence against an increase in capillary permeability in subjects exposed to high altitude
• Verf.angabe: Gian-Reto Kleger, Peter Bärtsch, Peter Vock, Bernhard Heilig, L. Jackson Roberts, Peter E. Ballmer
• E-Jahr: 1996
• Jahr: 1 November 1996
• Umfang: 7 S.
• Fussnoten: Gesehen am 17.01.2024
• Titel Quelle: Enthalten in: Journal of applied physiology
• Ort Quelle: Bethesda, Md. : American Physiological Society, 1948
• Jahr Quelle: 1996
• Band/Heft Quelle: 81(1996), 5, Seite 1917-1923
• ISSN Quelle: 1522-1601
• DOI: doi:10.1152/jappl.1996.81.5.1917
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: acute mountain sickness
• Sach-SW: F2-isoprostanes
• Sach-SW: free radicals
• Sach-SW: high-altitude pulmonary edema
• Sach-SW: vascular permeability
• K10plus-PPN: 1878299980

Abstract

Kleger, Gian-Reto, Peter Bärtsch, Peter Vock, Bernhard Heilig, L. Jackson Roberts II, and Peter E. Ballmer. Evidence against an increase in capillary permeability in subjects exposed to high altitude. J. Appl. Physiol.81(5): 1917-1923, 1996.—A potential pathogenetic cofactor for the development of acute mountain sickness and high-altitude pulmonary edema is an increase in capillary permeability, which could occur as a result of an inflammatory reaction and/or free radical-mediated injury to the lung. We measured the systemic albumin escape by intravenously injecting 5 μCi of125I-labeled albumin and the plasma concentrations of cytokines, F2-isoprostanes (products of lipid peroxidation), and acute-phase proteins in 24 subjects exposed to 4,559 m. Ten subjects developed acute mountain sickness, and four subjects developed high-altitude pulmonary edema. The transcapillary escape rate of albumin was 6.9 ± 2.0%/h (SD) at low (550 m) and 6.3 ± 1.9%/h at high (4,559 m) altitude (P= 0.23; n = 24). The subjects with high-altitude pulmonary edema had a modest but insignificant increase in the transcapillary escape rate of albumin (4.6 ± 1.9%/h at low vs. 5.7 ± 1.9%/h at high altitude;P = 0.42;n = 4). Plasma concentrations of fibrinogen, α1-acid glycoprotein, C-reactive protein, and interleukin-6 were unchanged in the early phases and significantly increased by the end of the observation period in the subjects with high-altitude pulmonary edema, whereas tumor necrosis factor-α and F2-isoprostanes did not change at all. This suggests that the inflammatory reaction was rather a consequence than a causative factor of high-altitude pulmonary edema. In summary, these data argue against a dominant role for increased systemic capillary permeability in the development of acute mountain sickness and high-altitude pulmonary edema.