Tissue remodeling during high-altitude pulmonary edema in rats: Biochemical and histomorphological analysis

High altitude characterized by the low partial pressure of the oxygen is a life-threatening condition that contributes to the development of acute pulmonary edema and hypoxic lung injury. In this study, we aimed to investigate the contribution of some inflammatory and oxidative stress markers along...

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Bibliographic Details
Published in:Tissue & cell 2025-04, Vol.93, p.102727, Article 102727
Main Authors: Shushanyan, Ruzanna A., Karapetyan, Hasmik M., Nadiryan, Edita E., Avtandilyan, Nikolay V., Grigoryan, Anna V., Karapetyan, Anna F.
Format: Article
Language:English
Subjects:
Antioxidant enzymes
Fibrosis
Inflammation
Mast cells
Oxidative stress
Pulmonary edema
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Summary:High altitude characterized by the low partial pressure of the oxygen is a life-threatening condition that contributes to the development of acute pulmonary edema and hypoxic lung injury. In this study, we aimed to investigate the contribution of some inflammatory and oxidative stress markers along with antioxidant system enzymes in the pathogenesis of HAPE (high-altitude pulmonary edema) formation. We incorporated the study on 42 male rats to unravel the role of mast cells (MCs) and TNF-α in the lung after the effect of acute hypobaric hypoxia. The HAPE model was mimicked with a decompression chamber at the altitude of 7620 m for a duration of 24 h. The study reveals various histological changes in the rat’s lung exposed to hypoxia that was accompanied by immense inflammatory cell infiltration, edema, hemorrhages, and fibrosis. Moreover, the wet weight of the lungs and the arginase level was also increased (p 
ISSN:0040-8166
1532-3072
1532-3072
DOI:10.1016/j.tice.2025.102727