Glucocorticoid response and adrenal lipid peroxidation in rats submitted to chronic hypobaric hypoxia.

The well known physiological changes that occur in adaptation to chronic hypobaric hypoxia (CHH) prevent the fall in arterial blood oxygen pressure below normal limits but neither the ventilatory nor the circulatory adaptation are able to maintain a normal capillary blood pO2. We report here our findings on adrenal histology, function, and lipid peroxidation in intact and castrated rats of both sexes submitted to twelve weeks of adaptation to 4,400 m simulated altitude. In the CHH rats hematocrit was increased; adrenal weight was increased in males and decreased in castrated females. Adrenal histology and histochemistry were normal. Corticosterone level and uric acid were unchanged except in castrated animals: corticosterone was decreased in males and increased in females. Uric acid was increased in castrated males, the only group in which adrenal lipid peroxidation was unaffected by castration. In the remaining groups, it was diminished compared to their intact controls. Intact normoxic males showed a significant direct correlation between plasmatic lipoperoxidation products (TBA-reactive substances) and uric acid (r = 0.961), which disappeared under hypoxia or with castration. Sex related differences were found in hematocrit and adrenal weight responses. The presence of androgens was involved in the adaptative response of cortical and reticular histometry, lipid peroxidation, and corticosterone level. These results do not support Selye's hypothesis of exhausted adrenal glands in chronic stages of adaptation and suggest that a proper relation between adrenal and gonadal steroids hormones is essential for systemic and tissular responses to diminished oxygen supply.