Raised HIF1α during normoxia in high altitude pulmonary edema susceptible non-mountaineers

Soree, Poonam ; Gupta, Rajinder K. ; Singh, Krishan ; Desiraju, Koundinya ; Agrawal, Anurag ; Vats, Praveen ; Bharadwaj, Abhishek ; Baburaj, T. P. ; Chaudhary, Pooja ; Singh, Vijay K. ; Verma, Saroj ; Bajaj, Amir Chand ; Singh, Shashi Bala (2016) Raised HIF1α during normoxia in high altitude pulmonary edema susceptible non-mountaineers Scientific Reports, 6 (1). ISSN 2045-2322

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Official URL: http://doi.org/10.1038/srep26468

Related URL: http://dx.doi.org/10.1038/srep26468

Abstract

High altitude pulmonary edema (HAPE) susceptibility is associated with EGLN1 polymorphisms, we hypothesized that HAPE-susceptible (HAPE-S, had HAPE episode in past) subjects may exhibit abnormal HIF1α levels in normoxic conditions. We measured HIF1α levels in HAPE-S and HAPE resistant (HAPE-R, no HAPE episode) individuals with similar pulmonary functions. Hemodynamic responses were also measured before and after normobaric hypoxia (Fi02 = 0.12 for 30 min duration at sea level) in both groups. . HIF1α was higher in HAPE-S (320.3 ± 267.5 vs 58.75 ± 33.88 pg/ml, P < 0.05) than HAPE-R, at baseline, despite no significant difference in baseline oxygen saturations (97.7 ± 1.7% and 98.8 ± 0.7). As expected, HAPE-S showed an exaggerated increase in pulmonary artery pressure (27.9 ± 6 vs 19.3 ± 3.7 mm Hg, P < 0.05) and a fall in peripheral oxygen saturation (66.9 ± 11.7 vs 78.7 ± 3.8%, P < 0.05), when exposed to hypoxia. HIF1α levels at baseline could accurately classify members of the two groups (AUC = 0.87). In a subset of the groups where hemoglobin fractions were additionally measured to understand the cause of elevated hypoxic response at baseline, two of four HAPE-S subjects showed reduced HbA. In conclusion, HIF 1 α levels during normoxia may represent an important marker for determination of HAPE susceptibility.

Item Type:Article
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Deposited On:04 Jul 2021 14:45
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