DESCRIPTION

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 < 0.05). While the NO level was shown to be diminished (p < 0.01). Acute hypobaric hypoxia also caused MC degranulation and increased TNF-α-expression in the lung, which considerably promoted inflammation after hypoxic damage.

However, the antioxidant system was weakened following the decreased activity of SOD and catalase. Moreover, the cell energy metabolism was also altered accompanied by an elevated level of LDH. Our findings suggest that the NO and arginase and antioxidant system enzymes along with TNF-α and MCs may play a role in HAPE pathogenesis and contribute to the alveolar-capillary barrier disruption that leads to edema formation.

Uncovering the pathological mechanisms of this disease would provide valuable information about the molecular basis of pulmonary edema development and therefore used for further preventive tools to manage the risks posed by high altitude-induced lung damage.

Back