2003 Volume 70 Issue 2 Pages 151-156
Intrauterine inflammation/infection has been associated with prenatal mortality and morbidity. However, few studies have been performed to investigate how the fetus responds to intrauterine inflammation/infection in utero. In the present study, fetal plasma prostaglandin (PG) F2α and cortisol responses to high-dose fetal endotoxin administration were evaluated in late gestation goats (n=8). After 160μg/kg of fetal weight of endotoxin (Escherichia coli, O111:B4 lipopolysaccharide) administration via the fetal jugular vein over a 5-min period, fetal plasma PGF2α and cortisol levels, fetal blood gases and pH were measured periodically.
After endotoxin administration, fetal plasma cortisol levels significantly increased to 9.5±0.8 ng/mL and 9.3±0.7 ng/mL after 1 and 3h, respectively (p<0.05) and plasma PGF2α levels did not change throughout the study. These results suggest that absent PGF2α and attenuated cortisol responses to high-dose fetal endotoxin administration, relative to the adult, may be a self-protective mechanism that diminishes premature delivery and fetal asphyxia.