Adrenal function and the incidence of bends after decompression in mice: effect of adrenalectomy, corticosteroids, decompression intensity, and time of day.

The adrenocortical endocrine subsystem has been demonstrated to enhance mammalian tolerance to harsh environmental conditions, including hypoxia and temperature extremes. In a series of factorial experiments, mice were exposed to one of three elevated hydrostatic pressures for 30 min and then decompressed (0.75 atm/s). It was demonstrated that 1) tolerance to decompression does not differ significantly (P greater than 0.3) in surgically intact, sham adrenalectomized, or in adrenalectomized animals; 2) intraperitoneal administration of pharmacologic doses (0.4, 1.0, and 2.0 mg/mouse) or corticosterone or deoxycorticosterone acetate does not significantly enhance (P greater than 0.1) survivorship when compared to vehicle-injected controls; and 3) the incidence of decompression sickness (DS) does not fluctuate with time of day (P greater than 0.4). In a fourth study, the plasma concentration of corticosterone was quantitated in 1) colony control mice, 2) mice exposed to the 1-ATA chamber environment (chamber control), or 3) mice compressed to 3, 5, 7, 9, or 11 ATA and then decompressed. In general, plasma corticosterone in symptom-free mice was elevated approximately threefold (P less than 0.05) by exposure to the 1-ATA chamber environment and by decompression from 3 to 11 ATA. At 11 ATA, plasma corticosterone levels in decompressed mice exhibiting decompression sickness symptoms were significantly elevated (P less than 0.05) compared to the levels observed in decompressed symptom-free mice. These studies indicate that adrenocortical function does not enhance tolerance to decompression in mice.