Exaggerated pulmonary hypertension is not sufficient to trigger high-altitude pulmonary oedema in humans

Details

Serval ID
serval:BIB_0D71DA3FE332
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Exaggerated pulmonary hypertension is not sufficient to trigger high-altitude pulmonary oedema in humans
Journal
Schweizerische Medizinische Wochenschrift
Author(s)
Sartori  C., Allemann  Y., Trueb  L., Lepori  M., Maggiorini  M., Nicod  P., Scherrer  U.
ISSN
0036-7672 (Print)
Publication state
Published
Issued date
03/2000
Volume
130
Number
11
Pages
385-9
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Mar 18
Abstract
High altitude pulmonary oedema (HAPE) is a paradigm of pulmonary oedema that occurs in otherwise healthy subjects and thereby allows us to study underlying mechanisms in the absence of damning factors. Exaggerated pulmonary hypertension, which is related at least in part to endothelial dysfunction, is a hallmark of high-altitude pulmonary oedema. It is thought to play an important part in the pathogenesis of HAPE, but the predisposing factors are not clear. In rats, transient exposure to hypoxia during the first few days of life predisposes to exaggerated hypoxic pulmonary vasoconstriction in adulthood. We hypothesised that a similar mechanism may operate in humans, and if so may predispose to high-altitude pulmonary oedema. To test this hypothesis we studied the effects of high-altitude exposure (4559 m) on pulmonary-artery pressure and incidence of pulmonary oedema in 10 healthy young adults who had suffered from transient hypoxic pulmonary hypertension during perinatal period, and compared these effects with those observed in 10 controls of similar age and sex distribution, and in 14 HAPE-prone mountaineers. We found that at high altitude, the subjects who had suffered from transient perinatal hypoxic pulmonary hypertension had exaggerated pulmonary hypertension compared to controls (62 +/- 7 vs 50 +/- 11 mm Hg, p < 0.01). Despite exaggerated pulmonary vasoconstriction of similar magnitude to that observed in HAPE-prone subjects (59 +/- 10 mm Hg), none of the young adults developed HAPE. In contrast, 8 of the 14 HAPE-prone subjects had radiographic evidence of lung oedema (p < 0.001 for the comparison with the other 2 groups). These data challenge previous concepts and indicate that exaggerated hypoxic pulmonary vasoconstriction, while consistently associated with HAPE, is not sufficient to trigger pulmonary oedema. This suggests that additional mechanisms play a role.
Keywords
Adult Altitude Sickness/complications/*physiopathology Animals Carbon Dioxide/blood Disease Susceptibility Echocardiography Female Forced Expiratory Flow Rates Humans Hypertension, Pulmonary/*complications/*physiopathology Male Oxygen/blood Pulmonary Edema/etiology/*physiopathology/radiography Rats Reference Values Retrospective Studies
Pubmed
Web of science
Create date
25/01/2008 15:00
Last modification date
20/08/2019 13:34
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