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After administration of ACTH it is possible to obtain traumatic deciduomata in rats ovariectomized during early pregnancy and delayed implantation in rats ovariectomized day 4 of pregnancy and injected dayly with oestradiol from day 8 or 9. The substance responsible seems to be Progesterone or Progesterone like corticoid.
In the rat oestrogen is essential for induction of implantation in a progesterone primed uterus. The ability of the catechol oestrogens, 4-hydroxy-oestradiol (4-OH-E2) and 2-hydroxy-oestradiol (2-OH-E2) to initiate the implantation process (blue reaction, indicative of increased endometrial capillary permeability at the location of the blastocyst) in hypophysectomized delayed implanting rats was compared to that of oestradiol-17 beta (E2). Delayed implantation was maintained by daily administration of 2 mg of progesterone. A single sc injection of 100 ng of E2 or 400 ng of 4-OH-E2 consistently initiated implantation in all animals. When delivered sc via osmotic minipumps at a constant release rate of 10 ng/microliters/h, implantation of a full complement of embryos was obtained with E2 given for 6 or 24 h. This dose 4-OH-E2 was ineffective when administered for 24 h. However, 25 ng/microliters/h for 24 h was effective. When the dose was increased to 50 ng/microliters/h implantation was evident in the majority of animals exposed to the hormone for 6 or 8 h; all animals implanted when this dose was given for 24 h. In contrast, 2-OH-E2 given at 50 ng/microliters/h for 24 h was totally ineffective. When the dose of the latter steroid was raised to 200 ng/microliters/h implantation was achieved in half of the animals when exposure was 24 h. The results suggest that when administered systemically, 4-OH-E2 is less potent than E2, but more potent than 2-OH-E2, for initiating implantation.(ABSTRACT TRUNCATED AT 250 WORDS)
A variation of the dye dilution technique was used to determine the volume of uterine fluid in 'implanting' and 'delayed implanting' mice. The method involves rinsing Krebs-Ringer-bicarbonate buffer containing [methyl-14C]methylated-BSA through the uterine lumen and using the resulting decrease in concentration of the BSA to calculate the volume of uterine fluid. The results indicated that the volume of uterine fluid was essentially the same in 'implanting' and 'delayed implanting' mice (i.e. 300-400 nl/pair of uterine horns). The total amounts of a substance recovered by rinsing the uteri would therefore provide an estimate of relative concentrations in situ.
The objective was the immunocytochemical localization of steroidogenic enzymes in the corpus luteum of Hokkaido brown bears during the period of delayed implantation. Cholesterol side-chain cleavage cytochrome P450 (P450scc), 3 beta-hydroxysteroid dehydrogenase (3 beta HSD), 17 alpha-hydroxylase cytochrome P450 (P450c17) and aromatase cytochrome P450 (P450arom) were localized as biosynthetic sites of pregnenolone, progesterone, androgens, and oestrogens, respectively. Ovaries containing corpora lutea were obtained from three mature bears during the expected delayed implantation period and ovarian sections were immunostained by the avidin-biotin-peroxidase complex method using polyclonal antibodies generated against steroidogenic enzymes of mammalian origin. P450scc and 3 beta HSD were localized in all luteal cells, whereas P450c17 (0.4-5.1% of 1000 cells) and P450arom (7.1-11.2% of 1000 cells) were localized in only a few luteal cells. These data suggest that luteal cells contain steroidogenic enzymes required for progesterone synthesis but also have a minimum capability for synthesizing androgen and oestrogen during the delayed implantation period in Hokkaido brown bears.
Heparin-binding EGF-like growth factor (HB-EGF) is a newly discovered member of the EGF family of growth factors. HB-EGF can bind to two loci on cell surfaces, heparan sulphate proteoglycans and EGF-receptor (EGF-R), and either one or both of these interactions could play a role in cell-cell interactions. In the rodent, increased endometrial vascular permeability at the site of blastocyst apposition is considered to be an earliest discernible prerequisite event in the process of implantation and this event coincides with the initial attachment reaction between the blastocyst trophectoderm and uterine luminal epithelium. This investigation demonstrates that the HB-EGF gene is expressed in the mouse uterine luminal epithelium surrounding the blastocyst 6-7 hours before the attachment reaction that occurs at 2200-2300 hours on day 4 of pregnancy. It was further demonstrated that this gene is not expressed in the luminal epithelium at the site of the blastocyst apposition during the progesterone-maintained delayed implantation, but is readily induced in the luminal epithelium surrounding an activated blastocyst after termination of the delay by an estrogen injection. In vitro studies showed that HB-EGF induced blastocyst EGF-R autophosphorylation, and promoted blastocyst growth, zona-hatching and trophoblast outgrowth. These results suggest possible interactions between the uterine HB-EGF and blastocyst EGF-R very early in the process of implantation, earlier than any other embryo-uterine interactions defined to date at the molecular level.
Cytophotometrics measures of DNA-Feulgen were realized in normal and delayed implantation blastocysts of the rat. During afternoon of the 5th day of progestation, blastocysts were of two types: those nuclei of which were in G1 gap and those nuclei of which were synthetising DNA. In delayed implantation, blastocyst nuclei were in G1 or G2 gap. Mitosis were rarely seen. After oestrogen injection DNA-synthesis started again. Cell kinetics before ovoimplantation is discussed.
The antigenicity of mouse blastocysts in experimentally delayed implantation and after activation from delay by estradiol administration were determined by two different methods. CBA blastocysts were incubated in C57BL/6J anti-CBA serum, and the amount of antibodies bound to the blastocysts was traced by -125-I-conjugated sheep antimouse gamma-globulin (isotope antiglobulin technique) and sensitized sheep red cells (mixed haemadsorption technique). With both techniques it was possible to demonstrate that mouse blastocysts in experimental delay of implantation possess alloantigens, and that this antigen expression has decreased markedly 14 hr after activation for implantation. It is suggested that this phenomenon may be of significance for noncognition of the allogeneic conceptus during pregnancy.
Urinary excretion of oestrone conjugates, pregnanediol-3 alpha-glucuronide (PdG) and 20 alpha-hydroxypregn-4-en-3-one were measured from 8 weeks before oestrus to 2 weeks post partum and bioactive FSH was monitored during the periovulatory interval in a female giant panda. A biphasic urinary bioactive FSH excretory profile appeared to indicate a broad (approximately 10 day) follicular phase followed by a sharp preovulatory bioactive FSH surge coincident with an acute increase in urinary oestrone conjugates and behavioural oestrus. Weekly concentrations of urinary oestrone conjugates and PdG increased (P less than 0.001) by Week 9 of gestation with 20 alpha-hydroxypregn-4-en-3-one levels increasing 10-30-fold (P less than 0.001) between Weeks 11 and 14. These observations indicate that the monoestrous giant panda does not appear to require a prolonged period of endogenous FSH release or multiple FSH peaks for ovarian priming and follicle selection to proceed normally. Furthermore, the delayed rise in urinary steroid excretion during the second half of gestation in the giant panda supports the concept of delayed implantation while the estimation of steroid conjugates in urine offers a non-invasive approach for monitoring pregnancy status in this endangered species.
PURPOSE: This study measured serum early pregnancy factor (EPF) in pregnant red deer (Cervus elaphus) and ascertained whether EPF synthesis is associated with implantation. METHODS: Serial serum samples were taken from mated hinds up to 42 days postconception and analyzed for EPF activity using the rosette inhibition test. EPF activity was then correlated with calving records and stages of preimplantation development. RESULTS: EPF was detected in all pregnant animals, with a twin pregnancy giving increased EPF activity. Three animals gave an EPF response following fertilization but failed to continue beyond the preimplantation embryo stage. The increase in EPF synthesis previously associated with implantation in other mammals occurred at the blastocyst stage in red deer. CONCLUSIONS: EPF synthesis in red deer (Cervus elaphus) is consistent with the preimplantation period, as occurs in other mammals. However, the second phase of the biphasic increase in early pregnancy factor production is associated with blastocyst formation, not implantation.
During pregnancy in mice, cell-mediated immunity as measured by a contact allergic reaction to picryl chloride was diminished (P less than 0.001). Mice in which delay of implantation was maintained by progesterone, and mice with progesterone- and oestradiol-maintained pregnancies, also showed a reduction in the inflammatory response. The response of pseudopregnant mice did not differ from that of the non-pregnant controls. Young mice sensitized before complete immunological competence gave a 50% response. The response doubled in animals given a second sensitization. The extent of the response in females with delay of implantation varied inversely with the dose of progesterone. A range of oestrogen doses gave the same depression in the response when given to pseudopregnant animals. Administration of HCG to pseudopregnant mice also reduced the inflammatory response.
To elucidate the action mechanisms of the IUD, I examined the relationships between ovarian steroid levels and contraceptive mechanisms in IUD-inserted rats. Female Wistar rats, 59-61 days old, were used and a polyethylene tube was into the bilateral uterine horns. Half of animals were injected with 1 mg indomethacin at the 30th and 31st days after the operation. All animals were decapitated at 1 hr after the 2nd injection. The presence of the IUD significantly increased the uterine weights due to the hypertrophy of the uterine wall, and it significantly increased ovarian testosterone and tended to increase ovarian estradiol and the estradiol/progesterone ratio. However, administration of indomethacin did not reduce these increased levels back to the levels of sham-operated rats. These results indicate that the presence of the IUD increased ovarian testosterone and estradiol, disturbing the balance between estrogen and progestin, with estrogen becoming dominant. It seems that these changes bring about the delay of fertilized egg development and disrupts the development of proper conditions for implantation, so that implantation of the fertilized egg on the endometrium is inhibited. Furthermore, this study suggests that the changes of the ovarian steroid levels in IUD-inserted rats may involve the participation of unknown uterine factors but not prostaglandins.
Embryonic development in Japanese long-fingered bats proceeded very slowly during and after the delayed implantation period (mid-October to mid-December). The primitive amniotic cavity and endoderm were formed before implantation. At the preimplantation stage (before hibernation) the corpus luteum cells appeared active, but became less active at the implantation stage (in hibernation). Activity was again apparent at the early placentation stage (after arousal).
Oestrogen action in the uterus is expressed in an early phase (Phase I) and a late phase (Phase II). The role of this biphasic oestrogen action in implantation is not clear. To determine the relative importance of Phase I and II responses, triphenylethylene compounds (CI-628, LY-117018, nafoxidine, clomiphene citrate and tamoxifen) and oestrogens (oestriol and oestradiol-17 beta) were used in a physiologically relevant experimental system for studying implantation. All compounds elicited uterine water imbibition to various degrees in ovariectomized-progesterone-treated mice at 6 h (Phase I response) and their effectiveness in inducing implantation in delayed implanting mice correlated with their respective potency to increase uterine wet weight. This suggests that Phase I might be an essential component of oestrogen action in implantation and that the efficiency of a compound to elicit a Phase I response might serve as a predictive indicator of its potential action on implantation.
The antifertility activity of piperine was investigated in pregnant mice when given by various routes of administration and at different periods of gestation. Piperine effectively inhibited implantation, produced abortion and delayed labor when it was given from day 2 through 5, day 8 through 12 and day 15 until labor, respectively. At the same dose level which interrupts pregnancy, piperine did not affect the estrous cycle. Neither uterotropic, antiestrogenic nor antiprogestational property was observed. Additionally, piperine also inhibited uterine contraction both in vivo and in vitro. These results suggested that the antifertility activity of piperine did not operate through any hormonal actions or uterotonic activity.
Uterine samples from Antechinus stuartii on days 1, 4, 6, 8, 11, 13, 15, 18, 21 and 23 after ovulation were examined histologically. Animals were pregnant, nonpregnant and unmated, or nonpregnant and mated but found to have only unfertilized eggs on autopsy. The histological parameters used were thickness of the myometrium, endometrial stroma, and endometrial epithelium, and density of uterine stromal glands and of lymphocytes at the endometrial basal lamina. Overall, the fluctuation patterns of these parameters were superficially similar between pregnant and nonpregnant animals (mated or unmated). However, statistically significant differences were detected between pregnant and unmated nonpregnant animals in every parameter examined at nearly every time point except day 13. Comparison of these results with known data on embryonic stages, corpus luteum development and plasma progesterone concentrations revealed that the gravid uterus underwent histological changes co-incident with changes in both progesterone concentration and developmental delay or embryonic arrest. It was concluded that the uterus mediates progesterone-driven changes in embryonic developmental rate. Although determination of number of lymphocytes provided inconclusive evidence of cellular immunity against embryos, the possibility that embryonic signalling to the uterus occurs is discussed.
A nonsteroidal antifertility agent 1,2-diethyl-1,3-bis(p-methoxyphenyl)-1-propene has been investigated to assess its capacity to induce implantation in delayed rats. The administration of the compound successfully induced the implantation in all rats. We have concluded that the process of induction of implantation in such rats may be due to a frank estrogenic action of the compound. Furthermore, the use of the compound as a new oral substitute for diethylstilbestrol is suggested.
Peripheral plasma progesterone concentrations exhibited an increase 10 days before implantation, coinciding with the resumption of blastocyst growth and with a decrease in plasma androgen values (DHA, androstenedione, testosterone). No definite pattern of oestrone was observed and oestradiol concentrations remained undetectable. The production of steroids by dispersed luteal cells showed that the growth of the corpora lutea paralleled that of blastocysts and resulted in hypertrophy followed by hyperplasia of the luteal cell. The production of progesterone in the medium increased with blastocyst size up to implantation; it was enhanced by mink charcoal-treated serum, but prolactin, LH, FSH or a combination of these hormones did not affect the progesterone production, whatever the stage of diapause. DHA and androstenedione secretion increased in the two last stages of blastocyst growth and was enhanced by LH. The conversion of androstenedione and testosterone into oestrone and oestradiol was observed at all stages of embryonic diapause, indicating that corpora lutea contain aromatase activity even at an early stage. The secretion of oestrone was higher than that of oestradiol. The non-luteal tissue contributed up to 50% of the steroid production; while progesterone and androgen production remained constant, that of oestradiol decreased at the end of the delay period. These results indicated a change in the size and the secretory capacity of the luteal cell related to blastocyst development and implantation. Although progesterone was the main product of the corpora lutea, androgens and oestrogens were also secreted.
Developmental delay is correlated with torpor in the temperate zone bent-winged bat, Miniopterus schreibersii (latitude 37 degrees S) as a period of pre-implantation delay (delayed implantation) followed by a short post-implantation delay (delayed development). During this time, the number of steroidogenic organelles in luteal cytoplasm is greatly reduced compared with normal embryogenesis, and granular endoplasmic reticulum is prominent. Nidation, which occurs while the animals are hibernating, is not accompanied by marked changes in luteal ultrastructure, although the number of lipid droplets decreases somewhat. Progesterone rises slightly but not significantly; however, a pre-nidation decrease in high 17 beta-estradiol levels may play a role in implantation. Following implantation, the conceptus remains delayed at the blastocyst stage for several weeks. During this time the bats remain torpid and the only change in luteal cell ultrastructure is an increase in smooth endoplasmic reticulum as differentiation begins toward the trilaminar stage. At the end of developmental delay hypertrophy of the luteal cell begins and mitochondria and lipid droplets increase, markedly. By this time arousal from hibernation has occurred, placentation takes place and normal development is underway. At placentation, smooth endoplasmic reticulum reaches its maximum in luteal cytoplasm; estrogen and progesterone levels peak about 6 weeks later. For the remaining 2 months of gestation, signs of luteolysis appear. These observations suggest that the corpus luteum of developmental delay, though sub-optimally functional, is prolonged in its luteinization by the arrival of winter when the bats enter torpor. The capacity for maximal steroidogenesis is acquired at the end of winter, some weeks after implantation, when arousal occurs and normal development ensues.