Studies were conducted to evaluate the changes in plasma concentrations of bovine fetal placental lactogen (bPL), insulin-like growth factor (IGF-I) and IGF-II following anti-bPL antibody infusion in fetal circulation. Abdominal aorta of bovine fetuses (n = 6) were chronically cannulated on the medial tarsal artery and infusion of rabbit anti-bPL IgG was performed during late gestation. From the first infusion, blood samples were collected from the fetus on a daily basis. Fetuses remained cannulated during the last 10 to 95 d of gestation. The time-series of hormonal data (bPL, IGF-I and IGF-II) were statistically analyzed for repeated measures as a split plot in time with number of anti-bPL infusions (one vs. more than one), dose of anti-bPL infused L (low, 4, 6, 8 mL) vs. H (high, 20 mL) and days after infusions (d 1 to d 7) as the fixed effects using the Mixed procedure of SAS (1998). IGF-I concentrations tended to reach a minimal concentration on d 3 after infusions (15.5 ± 3.4 ng/mL; P = 0.056). No changes were observed on IGF-II concentrations. The mean values of bPL on d 3 after infusion showed a significant increase. When low doses of anti bPL IgG were administered, no peak of binding in fetal serum was observed. When higher or repeated doses of anti bPL IgG were injected, a significant binding rate of the tracer (B/T) was recorded in the fetal serum during 1, 2 or several days. This high B/T can be due to circulating free anti bPL IgG; these rabbit IgG can remain in solution during the step of separation of free and bound fraction of the RIA and thus can bind part of the tracer and create an artifactual overestimation of the circulating bPL. However generally, concentrations of circulating bPL after anti bPL IgG injection were decreased justifying a transitory decrease in IGF-I concentrations. These data showed that following anti-bPL infusion, a transient decrease in IGF-I but not in IGF-II is observed. Our work suggests that PL somatogenic activities at the maternal-fetal interface are mediated through the IGF-I rather than IGF-II.