title: Endotoxemia in pregnant cows: Comparisons of maternal and fetal effects utilizing the chronically catheterized fetus.
abstract: We utilized the chronically catheterized bovine fetus to compare maternal and fetal responses to maternal lipopolysaccharide (LPS) infusion. Our hypothesis was that LPS-induced abortion was primarily a maternal luteolytic event with minimal transplacental fetal exposure. Fetal tibial arteries, amniotic, allantoic cavities and maternal carotid arteries were catheterized. Three cows had patent catheters with viable fetuses (190 to 200 days of gestation) 1 week after operation and were included in the study. Following a 2-day maternal and fetal baseline, 0.5 mug Salmonella typhimurium LPS/kg was infused into a maternal jugular vein over a 2-hour period. Maternal and fetal responses were monitored clinically, biochemically and hormonally. The maternal response consisted of marked increases in plasma prostaglandin F(2alpha) metabolite (PGFM), tumor necrosis factor (TNF), ACTH and cortisol with a dramatic maternal leucopenia within 2 hours. Progesterone concentrations decreased within 7 hours (P<0.05). The LPS was rapidly cleared from maternal circulation and no transplacental exposure was detected in the fetuses. Fetal responses to maternal endotoxemia consisted of increased ACTH and cortisol concentrations with delayed increases in PGE(2); TNF did not change in fetal fluids following maternal endotoxemia. There was a fetal leucocytosis within 2 hours. The results indicate that the fetus does not appear to play a major role in the pathogenesis of LPS-induced abortions. However, the role of maternal TNF in endotoxin abortion requires further study.
authors.affiliation: Department of Pathology, Cornell University, Ithaca, NY USA.
authors.forename: G L
authors.initials: GL
authors.lastname: Foley
authors.forename: D H
authors.initials: DH
authors.lastname: Schlafer
authors.forename: T H
authors.initials: TH
authors.lastname: Elsasser
authors.forename: M
authors.initials: M
authors.lastname: Mitchell