A systematic study of the daily concentrations of human chorionic gonadotropin (hCG) in maternal circulation following the time of probable implantation in 19 normal pregnancies was carried out. With the use of a specific antiserum to hCG β-subunit, significant increases in circulating hCG were observed by day 8 following the luteinizing hormone (LH) peak in 5.3% of cycles, by day 9 in 15.8%, by day 10 in 53.2%, and by day 11 in 100% of the cycles resulting in a normal pregnancy. After an initial rapid rise, mean plasma concentrations rose exponentially, with a doubling time of 1.3 days, to reach concentrations between 50 and 250 IU/l at the time of the first missed period. The time of detection of hCG was in close agreement with the anticipated time for this event estimated from morphologic studies. In three abnormal pregnancies, all of which ended in spontaneous abortion, hCG concentrations became progressively more abnormal from within 2 to 5 days of the appearance of this hormone in maternal plasma. Despite this, actual abortion did not occur for several days, or in one case for several weeks, after the divergence of hCG concentration from the normal range.
Mouse blastocysts were recovered from the uterus during experimental delay of implantation and following reactivation by estradiol and progesterone. The blastocysts were exposed to 7 different ferritin-conjugated lectins and then processed for electron microscopy. Binding of the lectins to the surface of the trophoblast was assessed by visualization of the ferritin particles using transmission electron microscopy. All lectins that have been previously shown to bind to trophoblast of predelay blastocysts also bound to blastocysts during delay and after reactivation from delay. The lectin from Dolichos biflorus (DBA), which does not bind to predelay blastocysts (ChÃ¡vez and Enders, 1981) began to bind to blastocysts as early as 24 h after ovariectomy and bound consistently throughout the duration of delay (5 days). Between 18-22 h after the administration of estradiol-17 beta and progesterone for reactivation (given on the 5th day of delay, i.e., Day 10 postcoitus [p.c.]) DBA binding sites disappeared from the surface of the trophoblast as the blastocysts became adherent to the uterine epithelium. Binding of DBA to delayed blastocysts was inhibited by N-acetylgalactosamine (NACGal) and also by treatment with N-acetylgalactosaminidase prior to exposure to the lectin. This indicates that NAcGal becomes available for DBA binding during delayed implantation and is subsequently cleaved off the glycocalyx or masked by the acquisition of other molecules that prevent binding of DBA following reactivation and during subsequent implantation of the mouse blastocysts. Since DBA binding was observed before the blastocysts became completely dormant and also after they became metabolically reactivated, DBA binding is probably not directly related to the state of implantation delay. However, the abolition of DBA binding occurred coincident with the blastocyst's adherence to the uterine epithelium and may be associated with the acquisition of adhesiveness.