Oxidative Stress and Histopathological Evaluation of Rat Lung Tissue during Hypobaric Hypoxia

Abstract

Hypobaric hypoxia (HH) is a condition associated with low partial pressure of oxygen in the atmosphere. This lowering of oxygen content in atmosphere leads to decreased circulating oxygen in the humans residing in these regions. This lowering of oxygen does not cause any serious complications in residents due to adaptation. On the other hand these extreme environments are challenging for high altitude (HA) sojourners as they develop range of illness from i.e. from mild altitude sickness to fatal diseases. Several studies have been carried on altitude environment to focus physiological complications and adaptation. Serum-based clinical studies are comparatively easy due to availability of human volunteers. Tissue-based studies are still challenging as the development of animal model is the only approach. Herein we report lung tissue based oxidative stress markers level in conjunction with histopathological findings in rodent model. Male Wistar rats were exposed to 338 mm Hg pressure, simulating an altitude of 15,000ft in decompression chamber. Animals were used exposed for different durations i.e. 2 h, 4h, 8h, 12h, 16h, 24 h and 48 h (n=9/group). Partial pressure of oxygen (PO2) and carbon dioxide (PCO2) in arterial blood of animals were checked to confirm induction of hypoxia. Decreased value of PO2 and PCO2 during different exposure groups confirmed successful induction of hypoxia in animals. Altered valve of superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), lipid peroxidation (LPO) and reduced glutathione (GSH) in lung tissue of these groups confirmed occurrence of oxidative stress. Lung histopathological analysis of hypoxic groups provided evidence of lung injury on prolonged exposure. Short term hypoxic exposure (2h-4h) did not showed any major effect on lung architecture but with increased duration of exposure (8h-16h) deformities in lung parenchyma were observed, leading to development edema during 24h-48h of exposure. Alteration in oxidative stress markers during 12h-16h can be correlated with common altitude sickness which on prolong exposure (24h-48h) can turn into serious complication like pulmonary edema.