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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 µg/100 ml 1 h after operation. By 24 h after operation, levels had fallen back to 7·6 µg/100 ml. In the pregnant mouse an acute surgical stress on day 14 of pregnancy increased plasma corticosterone levels to 525 µg/100 ml 1 h after surgery from a resting value of 80 µg/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 µg/100 ml) 1 h after the start of restraint and were still raised (mean 24·0 µg/100 ml) after 24 h. In the pregnant restrained mouse a peak value of 733 µg/100 ml was seen at 1 h, with levels maintained at around 500–600 µg/100 ml during the next 16 h of restraint. Increased levels of 268 µg/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 fooddeprived 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 µg/100 ml were maintained for some hours, protein binding studies indicated that 10 µg/100 ml was free, unbound corticosterone. The physiological and pathological consequences of such high levels of free corticosterone during stress in pregnancy are discussed.

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