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Exaggerated pulmonary hypertension is not sufficient to trigger high-altitude pulmonary oedema in humans.
Schweiz Med Wochenschr 2000; 130(11):385-9SM

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.

Authors+Show Affiliations

Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, Lausanne.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10774001

Citation

Sartori, C, et al. "Exaggerated Pulmonary Hypertension Is Not Sufficient to Trigger High-altitude Pulmonary Oedema in Humans." Schweizerische Medizinische Wochenschrift, vol. 130, no. 11, 2000, pp. 385-9.
Sartori C, Allemann Y, Trueb L, et al. Exaggerated pulmonary hypertension is not sufficient to trigger high-altitude pulmonary oedema in humans. Schweiz Med Wochenschr. 2000;130(11):385-9.
Sartori, C., Allemann, Y., Trueb, L., Lepori, M., Maggiorini, M., Nicod, P., & Scherrer, U. (2000). Exaggerated pulmonary hypertension is not sufficient to trigger high-altitude pulmonary oedema in humans. Schweizerische Medizinische Wochenschrift, 130(11), pp. 385-9.
Sartori C, et al. Exaggerated Pulmonary Hypertension Is Not Sufficient to Trigger High-altitude Pulmonary Oedema in Humans. Schweiz Med Wochenschr. 2000 Mar 18;130(11):385-9. PubMed PMID: 10774001.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exaggerated pulmonary hypertension is not sufficient to trigger high-altitude pulmonary oedema in humans. AU - Sartori,C, AU - Allemann,Y, AU - Trueb,L, AU - Lepori,M, AU - Maggiorini,M, AU - Nicod,P, AU - Scherrer,U, PY - 2000/4/25/pubmed PY - 2000/5/20/medline PY - 2000/4/25/entrez SP - 385 EP - 9 JF - Schweizerische medizinische Wochenschrift JO - Schweiz Med Wochenschr VL - 130 IS - 11 N2 - 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. SN - 0036-7672 UR - https://www.unboundmedicine.com/medline/citation/10774001/Exaggerated_pulmonary_hypertension_is_not_sufficient_to_trigger_high_altitude_pulmonary_oedema_in_humans_ L2 - http://www.diseaseinfosearch.org/result/6088 DB - PRIME DP - Unbound Medicine ER -