Search

Plasma corticosterone levels were measured in the pregnant and non-pregnant mouse after acute and chronic stress. Acute surgical stress in the non-pregnant mouse increased plasma corticosterone from a mean resting level of 2-3 to 50-6 mug/100 ml 1 h after operation. By 24 h after operation, levels had fallen back to 7-6 mug/100 ml. In the pregnant mouse an acute surgical stress on day 14 or pregnancy increased plasma corticosterone levels to 525 mug/100 ml 1 h after surgery from a resting value of 80 mug/100 ml, with a return to resting levels by 24 h. During the chronic stress of 24 h restraint, plasma corticosterone levels in the non-pregnant mouse reached a peak (81-0 mug/100ml) 1 h after the start of restrain and were still raised (mean 24-0 mug/100 ml) after 24 h. In the pregnant restrained mouse a peak value of 733 mug/100 ml was seen at 1 h, with levels maintained at around 500-600 mug/100 ml during the next 16 h of restraint. Increased levels of 268 mug/100 ml were still present at 24 h. After the chronic stress of 24 h food deprivation, plasma corticosterone levels in the non-pregnant and pregnant mice were raised after 7 h to levels slightly lower than those observed in the restrained groups, and at 24 h levels in the respective restrained and food-deprived groups were similar, suggesting that food deprivation is a powerful chronic stressor in the mouse. During chronic stress in the pregnant mouse where plasma corticosterone levels of around 600 mug/100 ml were maintained fro some hours, protein binding studies indicated that 10 mug/100 ml was free, unbound corticosterone. The physiological and pathological consequences of such high levels of free corticosterone during stress in pregnancy are discussed.

Stress or administration of ACTH to pregnant mice gave rise to much higher plasma corticosterone levels in the second half of pregnancy than in the first half, suggesting that there may be increased adrenal sensitivity to ACTH or decreased metabolism of corticosterone during the second half of pregnancy.

The effect of daily, oral administration of diazepam on plasma corticosterone responses to stressors of varying intensity was investigated. In rats exposed to the mild stress of noise, diazepam, 10 mg kg-1 but not 1.0 or 0.1 mg kg-1, reduced plasma corticosterone concentrations by 30% in comparison with controls. However, in rats exposed to the more severe stressors, foot-shock or immobilization, none of these doses of diazepam reduced plasma corticosterone responses. In unstressed rats, diazepam 10 mg kg-1 raised plasma corticosterone concentrations. It is suggested that plasma corticosterone concentrations are not a reliable indicator of the tranquillizing effect of diazepam during stress.

The blood level of corticosterone was measured in mice following the injection on day 14 of pregnancy of a dose of corticosterone sufficient to cause a low frequency of cleft palate in the fetuses. This was compared with the blood levels present during maternal restraint and food deprivation that produced a similar frequency of cleft palate. The mean blood level over the 24 h following injection of corticosterone was 660 mug/100 ml, and during a similar period of restraint was 485 mug/100 ml. Other mice were subjected either to restraint or food deprivation for 24 h beginning day 14 of pregnancy, the plasma corticosterone levels measured during that time, and the frequency of cleft palate in late fetuses compared with the individual plasma corticosterone levels during treatment. There was a significant (P less than 0.025) correlation between high maternal corticosteroid levels and the frequency of cleft palate in the offspring of the restrained mice but not in the food-deprived animals. It is suggested that in some stressed mice endogenous plasma corticosterone can reach levels sufficient to account for the development of cleft palate.