A GIRL was born on July 25, 1978, as a result of in vitro fertilization and embryo transfer. 1 After that, a boy was born in England through the efforts of the same investigators, 2 and more recently a girl was born in Australia through the efforts of an independent team. Another girl may also have been born in India. The birth of the first of these babies caused worldwide publicity that led simultaneously to acclaim and concern. The acclaim greeted the development of another technique to treat barrenness due to blocked fallopian tubes — one of the common and intractable causes . . .
The purpose of this experiment was to determine whether prolactin (PRL) is the factor that activates the quiescent corpus luteum (CL) and terminates the delay that precedes implantation in mink. Animals were hypophysectomized or sham-hypophysectomized 6 days after the second of two matings. Eight hypophysectomized mink received 0.5 mg ovine PRL (NIH-P-S13) daily through Days 21-24 of the experiment (Day 0 = day of surgery). Five sham-hypophysectomized and one hypophysectomized animal received no hormone therapy after surgery. All animals were bled at 3 day intervals until termination by exsanguination between Days 21 and 24. Uteri were observed by means of midventral laparotomy between Days 14 and 16. The hypophysectomized, untreated mink displayed neither luteal activation nor embryo implantation throughout the duration of the experiment. In hypophysectomized mink injected with PRL, luteal activation, as indicated by an increase in peripheral progesterone above pretreatment levels, had begun by Day 3 and persisted through Day 15 (P<0.05). Uterine swellings were present in six of eight PRL-treated mink at Days 14-16 and in seven of eight at Days 21-24. These swellings were found to contain implanted embryos at necropsy. Luteal activation occurred by Day 9 in sham-hypophysectomized mink, and progesterone continued to increase through Day 24. No evidence of implantation was present at Days 14-16 in this group but three of five had implanted by Days 21-24. The results demonstrate that PRL alone will induce luteal activation and embryo implantation in hypophysectomized mink. However, PRL alone appeared not to be able to sustain luteal function. It is suggested that photoperiod acts through hypophyseal PRL secretion to terminate embryonic diapause in mink.
Implantation in the rabbit occurs between 156-168 h postcoitum (p.c.), and by 175 h p.c. implanting blastocysts cannot normally be flushed intact from the uterine lumen. The effect of an intraluminal injection of DL-Î±-methylhistidine (DL-Î±-MH), a specific inhibitor of histidine decarboxylase, on implantation in the rabbit was studied. An intraluminal injection of 2.5 mg of DL-Î±-MH at 102 h p.c. interfered with implantation in the rabbit sacrificed at 175 h p.c. Implantation rates were reduced by more than 60% and this was reflected in the increased number of morphologically expanded normal blastocysts which were flushed from the uterine lumen intact. On the other hand, the same treatment did not significantly reduce the number of embryos implanted nor the viability of fetuses when examined on Day 12. However, 4 mg of DL-Î±-MH drastically reduced the implantation rates as well as the viability of the implanted embryos on Day 12. The intraluminal injections of various doses of L-histidine did not significantly affect the implantation rates or the viability of the fetuses. These results as well as our previous findings suggest that implantation may have been delayed for some time due to inhibition of embryonic histamine synthesis by DL-Î±-MH.
Scanning and transmission electron microscopic observations were made on trophoblast, caruncles and intercaruncular areas during the attachment of the conceptus. Three stages were determined: Between the caruncles, the trophoblast developed finger-like villi which invaded the lumen of the uterine glands from days 15 to 18. During their short life-time (they vanish at day 20), these trophoblastic differentiations may anchor the pre-attachment conceptus and absorb the histotrophic secretions of the glands.
Using three congenic strains, C57BL/10Sn(H-2b), B10.A/SnSg(H-2a), and B10.D2/nSn(H-2d), we sought to investigate the possible association of H-2 haplotype with the number of implants, fetal survival, and fetal weight, as well as to analyze the possible effects of hybrid vigor and maternal-fetal histoincompatibility in primigravidae mice. The results of this study indicate a significant association between genes at or near the H-2 complex and both fetal loss and fetal weight, but not the number of implants. Haplotype variation accounted for 14 percent of the variation in fetal loss and 20 percent of the variation in fetal weight. With the exception of fetal loss, there was no evidence of a maternal effect. There was also no clear evidence of hybrid vigor or histoincompatibility effects for any of the three variables studied. In summary, the data suggests that particular allelic variants at or near the H-2 complex confer some selective advantage as measured by differential fetal survival and fetal growth.
Immature Sprague-Dawley rats were maintained with lights off between 1900 and 0500 h and treated with pregnant mare serum gonadotropin (PMSG) at 30 days of age (0800-0900 h, Day 0). One hundred and ninety-eight animals were caged individually with mature fertile males at 1500 h on Day 2, scored for the occurrence of mating on the morning of Day 3, and killed on Day 22. Rats received 4, 8, 16, or 40 IU PMSG; a high proportion of those receiving each dose mated. Of those which mated, almost all receiving 4 or 8 IU, 76% of those receiving 16 IU, and none receiving 40 IU were pregnant on Day 22. The mean numbers of live fetuses in pregnant rats that received 4, 8, and 16 IU PMSG were 8.8, 12.9, and 14.2, respectively. The corresponding means for numbers of implanted embryos were 9.7, 15.4, and 18.8; for numbers of corpora lutea of pregnancy (CLP), 10.8, 20.8, and 48.1; for fetal weight, 2.25, 1.65, and 1.38 g; for placental weight, 0.47, 0.38, and 0.36 g; for peripheral serum estradiol concentration, 104, 125, and 112 pg/ml; and for peripheral serum progesterone concentration, 91, 112, and 164 ng/ml. Serum estradiol levels were more correlated to numbers of live fetuses than to numbers of CLP (r = 0.32, 0.01
When tested in protein-free medium NCTC 109, mouse blastocyst hatching in vitro was inhibited by low doses (<50 ÂµM) of indomethacin, meclofenamic acid, mefenamic acid, and naproxen. Ketoprofen was not inhibitory within the same concentration range. In medium supplemented with 10% fetal calf serum, meclofenamic acid inhibited hatching above 100 ÂµM but in contrast naproxen had no effect at 500 ÂµM. By ultrafiltration plus HPLC analysis, it was found that for meclofenamic acid over the range 100-200 ÂµM, 92-83% was bound to 10% fetal calf serum. Cinemicrographic recording of supplemented cultures containing 100 to 150 ÂµM meclofenamic acid revealed that the principal reason for the inhibition of hatching was the prevention of adequate blastocyst expansion which is a normal prerequisite to hatching in vitro. Intrauterine administration of 160 ÂµM meclofenamic acid to one horn of pregnant mice on Day 4 significantly reduced the rate of implantation.