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ARS Home » Research » Publications at this Location » Publication #61040


item Klemcke, Harold

Submitted to: Biology of Reproduction
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/15/1995
Publication Date: N/A
Citation: N/A

Interpretive Summary: Studies are being conducted to evaluate the role of glucocorticoids (steroidal hormones from the adrenal gland) in porcine fetal development and survival. As part of these studies, it is important to know if the glucocorticoids come from only the fetus or both the mother and fetus. Hence, an experiment was conducted to 1) determine whether maternal cortisol, a specific glucocorticoid, can pass across the placenta and contribute to cortisol in the fetal blood; 2) determine the effect of gestational age on this passage; and 3) calculate the percent contribution of maternal to fetal cortisol. Pregnant pigs were infused with radioactive cortisol at 50 and 100 days of gestation (term = 114 days). Blood samples were collected, steroids purified, and the amount of radioactivity present in cortisol in maternal and fetal blood determined. Indeed, low amounts of radioactive maternal cortisol did cross the placenta into fetuses. At 50 days, maternal cortisol accounted for 23% of fetal cortisol. This contribution dropped to 6% at 100 days. Hence at these gestational ages, the fetus itself is the primary source of fetal cortisol. The placenta appears to represent a "barrier" to passage of maternal cortisol to the fetuses. Because in some species high fetal glucocorticoids slow fetal growth, factors contributing to this placental barrier would, therefore, be important in maintaining low amounts of glucocorticoids, such as cortisol, in fetal blood and ensuring appropriate fetal development.

Technical Abstract: An experiment was conducted to determine the source of fetal cortisol at 50 (n = 5) or 100 days (n = 4) of gestation (term = 114 days). Equilibrium concentrations of tritiated cortisol were achieved, and all hormonal measures were made at 110, 130, 140, and 150 min in anesthetized pigs. Maternal plasma cortisol did not differ (p = 0.48) between 50 (70.2 +/- 7.4 4ng/ml; mean +/- SEM) and 100 days (62.4 +/- 5.8 ng/ml). Conversely, fetal cortisol increased (p = 0.048) between 50 (8.5 +/- 2.5 ng/ml) and 100 days (24.2 +/- 4.2 ng/ml) and, at each gestational age, was lower (p = 0.001) than those in maternal plasma. Plasma cortisone (15.1 +/- 2.3 ng/ml) did not change with gestational age (p = 0.42) in either compartment (maternal or fetal plasma), nor did it differ between compartments (p = 0.08). Maternal cortisol accounted for 22.8 +/- 2.0% of fetal cortisol at 50 days of gestation, and this contribution decreased (p < 0.00 1) to 5.87 +/- 0.8% %at 100 days. At both ages, maternal cortisol accounted for almost 50% of fetal cortisone. Metabolism of maternal cortisol by the entire uterofeto- placental unit was 16.8 +/- 3.4% at 50 days and 15.0 +/- 4.7% at 100 days (p = 0.76). Maternal MCR of cortisol increased 44% (p = 0.003) between 50 and 100 days (1.49 +/- 0.4 vs 2.15 +/- 0.2 liters/min). Hence at these gestational ages, the fetus--presumably the fetal adrenal--is the primary source of fetal plasma cortisol. The major contribution of maternal cortisol to fetal cortisone strongly suggests the presence of porcine placental 11beta-hydroxysteroid dehydrogenase activity. Further, factors constituting the placental "barrier" that metabolize maternal cortisol to cortisone and other products may be major regulators of porcine fetal plasma cortisol and cortisone.