SUMMARY Plasma corticosterone levels were measured throughout pregnancy and on the first day post partum in the mouse. During the first half of pregnancy plasma corticosterone levels rose from the non-pregnant value of 2·3 μg/100ml to 15·2 μg/100 ml on day 10. During the second half of pregnancy there was a sharp rise, levels reaching a peak of 138·3 μg/100ml on day 16. Following parturition there was a rapid fall to 18·3 μg/100 ml on the morning of the first day post partum. Adrenalectomy on day 15 resulted in an 80% fall in plasma corticosterone levels indicating that most of the steroid was of adrenal origin. The remaining portion of the corticosterone was found to be of foeto-placental origin, and in the chronically adrenalectomized animal this source was capable of maintaining high blood levels of corticosterone (67 μg/100 ml). The foeto-placental unit also provides the main secretory stimulus to the adrenal gland, but the mechanism by which it does this is not understood.
Background-Familial hiatal hernia has only rarely been documented. Aims-To describe the pattern of inheritance of familial hiatal hernia within an aVected family. Subjects-Thirty eight members of a family pedigree across five generations. Methods-All family members were interviewed and investigated by barium meal for evidence of a hiatal hernia. Results-Twenty three of 38 family members had radiological evidence of a hiatal hernia. No individual with a hiatal hernia was born to unaVected parents. In one case direct male to male transmission was shown. Conclusions-Familial inheritance of hiatal hernia does occur. Evidence of direct male to male transmission points to an autosomal dominant mode of inheritance. (Gut 1999;45:649-652)
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.
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