Effect of pelvic endometrial implants on overall reproductive functions of female rats. (1/464)

The effects of pelvic endometrial implants on the overall reproductive potential of female rats were investigated. After homologous transplantation in the peritoneum, the ectopic endometrium developed into highly vascularized nodes that gradually increased in mass until the 9th week postsurgery and then plateaued. In the presence of these implants, overall reproductive function was adversely affected. The effect was of greatest magnitude during 50-70 days posttransplantation. As compared with values in corresponding controls, ovulation was reduced by 43% (6 of 14) (p < 0.05), mating rate was reduced by 44% (12 of 27) (p < 0.025), and premature termination of pregnancy occurred in 34% (5 of 15) of rats. Wastage of pregnancy, which included complete termination or reduction of fetal number, occurred during the postimplantation course of gestation. Furthermore, 100% of the rats with transplants failed to respond to the copulomimetic stimulation for the induction of pseudopregnancy (p < 0.01, compared with corresponding controls). However, on exposure to vasectomized males, 46% (6 of 13) of these rats exhibited development of pseudopregnancy (p < 0.05, compared with corresponding group receiving copulomimetic stimulation). Increased rate of mating failure and differential pseudopregnancy rates after copulomimetic and natural cervical stimulation suggest that the rats with endometrial explants possibly had an absence or a short appearance of behavioral estrus. Hormonal assessment during the preovulatory phase showed a tendency toward lower mean levels of preovulatory estradiol and significantly lower LH (p < 0.01) and progesterone (p < 0.01) concentrations. The adversely affected reproductive functions may be a secondary consequence of these altered endocrine milieus.  (+info)

Natural cytotoxic and antibody-dependent cellular cytotoxic activity of cells in the decidua basales and metrial glands of pseudopregnant rats with deciduomata. (2/464)

Cytotoxic cells are present in the uterine wall of pregnant rats. To determine if the cytotoxic activity arises in response to semen or the products of conception, the profile of cytotoxic activity in deciduomata of pseudopregnant rats was examined. To examine NK activity, Yac-1 cells were used as targets in chromium release cytotoxicity assays and an antibody to Yac-1 cells was included in some assays to determine antibody-dependent cellular cytotoxic (ADCC) activity. Cells from the metrial glands and deciduae of deciduomata of rats at days 10 and 13 of pseudopregnancy did not show NK activity but ADCC activity was present. To examine natural cytotoxic (NC) activity, Wehi 164 cells were used as targets in chromium release cytotoxicity assays. Cells isolated from the metrial glands and deciduae of rats at day 10 of pseudopregnancy were able to kill Wehi 164 cells after 21 h assays, thus demonstrating NC activity. The profile of cytotoxic activity in the uterine wall of pseudopregnant rats with deciduomata is similar to that found in pregnancy and is thus independent of semen or the products of conception.  (+info)

Induction of pseudopregnancy in the mongolian gerbil (Meriones unguiculatus) by vaginal stimulation. (3/464)

In rats, pseudopregnancy has been induced by mating with vasectomized males, by mechanical stimulation of the uterine cervix with a glass rod or vibrator, and by stimulation of the vagina with a tampon. On the other hand, no practical data are available in reports on the induction of pseudopregnancy in Mongolian gerbils. Pseudopregnancy of gerbils has been induced by mating with vasectomized males. But this method was uncertain because the incidence of pseudopregnancy was lower than that obtained in rats by other means. In the present study, two experiments were undertaken as follows. 1) Copulatory behavior of gerbils was observed for one hour to determine the most effective stimulation interval. 2) From the results of Experiment 1, female gerbils in estrus were mechanically stimulated to test the effectiveness of inducing pseudopregnancy by vaginal stimulation at various time intervals. The results of these experiments indicated that, although the frequency of copulatory behavior varied among individuals, on average the most effective method for inducing pseudopregnancy was stimulation of 5 min duration and at 20 or 30 min intervals. Because the incidence of pseudopregnancy induced by such mechanical stimulation (83.3%) was higher than that induced by mating with vasectomized males (30.0%), this method might be useful in inducing pseudopregnancy in Mongolian gerbils.  (+info)

FSH inhibits the augmentation by oestradiol of the pituitary responsiveness to GnRH in the female rat. (4/464)

The effect of follicle stimulating hormone (FSH) treatment on the pituitary response to gonadotrophin-releasing hormone (GnRH) was studied in rats in various reproductive conditions. A 3-day treatment of cycling rats with FSH (Metrodin; 10 IU/injection) lowered the spontaneous pre-ovulatory. LH-surge and suppressed the pituitary luteinizing hormone (LH) response to GnRH. FSH also suppressed the LH response of pseudopregnant (PSP) rats on day 8 of pseudopregnancy, but not that of day-8 PSP rats which had been ovariectomized on day 4 (OVX-PSP rats). GnRH induced self priming in cycling, PSP and OVX-PSP rats. Oestradiol strongly augmented the pituitary LH-response to GnRH injection in PSP and OVX-PSP rats, but not in cycling rats; probably because in these latter animals the LH response to GnRH was already augmented by endogenous oestradiol. FSH suppressed the LH response to GnRH in oestradiol-treated PSP and cycling rats; in these latter rats the suppression of the LH response was as strong as that in cycling rats not treated with oestradiol. FSH did not suppress the LH response of oestradiol-treated OVX-PSP rats. The effect of FSH was not associated with changes in plasma oestradiol and progesterone concentrations. Analysis of the data revealed that FSH specifically suppressed the augmentative effect of oestradiol, but did not affect the GnRH-self priming effect. It is concluded that under the influence of FSH, the ovaries produce a factor which suppresses the augmentative effect of oestradiol on the GnRH-induced LH response of the pituitary gland. It is suggested that this effect of FSH underlies the suppression of the spontaneous LH-surges of FSH-treated cycling rats. As the present putative 'oestrogen-antagonizing factor' did not suppress the GnRH-self priming effect, it is suggested that this factor is not identical to gonadotrophin surge inhibiting factor.  (+info)

Embryo-dependent induction of embryo receptivity in the mouse endometrium. (5/464)

The effect of intraoviductal embryos on endometrial receptivity was studied by intraendometrial and intrauterine embryo transfer. Five-week-old female ICR mice were mated after superovulation; a vaginal plug confirmed day 1 of pregnancy. On day 4 (90 h after hCG injection), blastocysts were collected and transferred to pseudopregnant female mice and to recipient mice in which the uterotubal junction had been ligated bilaterally on day 1 of pregnancy. Three embryos per uterine horn, a total of six embryos per recipient mouse at days 1-6, were transferred to the endometrium or uterine cavity and implantation and pregnancy rates were calculated. The implantation rate for intraendometrial embryo transfer to recipients of days 3, 5 and 6 was significantly higher for uterotubal junction-ligated mice (72.2, 20.8 and 9.7%, respectively) than for pseudopregnant mice (55.0, 8.3 and 0.0%, respectively). The implantation rate for intrauterine embryo transfer to recipients at days 2, 5 and 6 was significantly higher for uterotubal junction-ligated mice (11.1, 25.0 and 8.3%, respectively) than for pseudopregnant mice (0.0, 3.3 and 0.0%, respectively). Uterotubal junction-ligated mice achieved implantation and bore neonates by intrauterine embryo transfer on days 2 and 6, whereas no implantation was achieved in pseudopregnant mice. The difference in implantation rate could not be explained by a difference in progesterone concentration between the groups. The distribution of proliferating cells in the endometrium was also studied immunohistochemically by use of anti-proliferating cell nuclear antigen (PCNA) antibody in the recipient mice. PCNA-positive cells were more abundant in uterotubal junction-ligated mice and demonstrated a marked extension from the epithelium to the stroma over time, in contrast to those in pseudopregnant mice. These findings indicate that an intraoviductal embryo exerts a biological effect by sending a signal to the endometrial epithelium and stroma, thus facilitating endometrial receptivity to the embryo and improving the rate of implantation.  (+info)

26-cholesterol hydroxylase in rat corpora lutea: A negative regulator of progesterone secretion. (6/464)

From a subtracted cDNA library of rat luteal tissue, where cDNA fragments in functional luteal tissue were subtracted from those in regressing luteal tissue, a cDNA clone corresponding to 26-cholesterol hydroxylase (P450(C26)) was obtained. It is known that P450(C26) catalyzes the conversion of cholesterol to 26-hydroxycholesterol, which blocks cholesterol utilization in the cell, and that 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) catalyzes the conversion of progesterone to an inactive steroid, 20alpha-dihydroprogesterone (20alpha-OHP). Thus, using pseudopregnant rats as a model, physiological cooperation of P450(C26) and 20alpha-HSD in the reduction of progesterone release toward the end of the luteal phase was evaluated. Levels of P450(C26) and 20alpha-HSD mRNA were examined in corpora lutea from pseudopregnant rats by Northern blot or reverse transcription-polymerase chain reaction or both. P450(C26) mRNA was ubiquitously expressed in corpora lutea, and its expression increased toward the end of pseudopregnancy, while 20alpha-HSD was expressed in all corpora lutea on Day 16 (Day 0 = the day of after cervical stimulation) but not detected before Day 10. An inhibitor of 20alpha-HSD, STZ26 (D-homo-16-oxa-4-androstene-3,16alpha-dione), was administered at various doses to rats from Day 12 to 20, effectively suppressing the elevation of 20alpha-OHP in a dose-dependent manner but not the depletion of progesterone completely. The expression of P450(C26) mRNA was increased as STZ26 dose increased, which negatively correlated with the progesterone levels. These results strongly suggest that P450(C26) cooperated with 20alpha-HSD in the reduction of progesterone release from the rat luteal tissue at the end of the functional luteal phase.  (+info)

Biphasic change in correlation between ovarian lipid peroxides and progestational activity during pseudopregnancy induced in immature rats. (7/464)

We measured ovarian lipid peroxide (LP) levels and plasma progestins, progesterone (P4) and 20alpha-dihydroprogesterone, throughout pseudopregnancy in gonadotropin-primed immature rats. Plasma P4 fluctuated, with two peaks on days 5 (PSP5) and 8 of pseudopregnancy, and then declined to the basal level by PSP12. Ovarian LP increased from PSP1 to PSP4, decreased temporarily until PSP8, and then rose gradually until PSP14. From PSP1 through PSP7, ovarian LP was positively correlated with total progestins according to the Spearman ranked correlation coefficient (r=+0.829, p<0.05). In contrast, a negative correlation between ovarian LP and plasma P4 was apparent (r=-0.816, p<0.05) from PSP8 to PSP14. These results show the biphasic correlation of LP with luteal progestational activity depending on the luteal stage.  (+info)

Technical note: use of slow-release estradiol and prostaglandin F2alpha to induce pseudopregnancy and control estrus in gilts. (8/464)

We determined whether a single injection of slow-release estradiol-17beta (SRE2) would induce pseudopregnancy in gilts and whether PGF2alpha would regress the corpora lutea (CL) of pseudopregnancy. Crossbred gilts (n = 40) were induced to ovulate by treatment with 400 IU of hCG + 200 IU of eCG (PG600, Intervet, Millsboro, DE) given at 180 d of age (d = 0). On d 14, gilts were injected i.m. with one of five doses (n = 8 gilts/dose) of SRE2 (0, 12.5, 25, 50, or 100 mg). Blood samples were collected before SRE2 and twice weekly until d 73 to monitor serum progesterone (P4) and estradiol (E2). On d 59, gilts received (i.m.) 10 mg of PGF2alpha (Lutalyse, Pharmacia Upjohn, Kalamazoo, MI) and were checked for estrus for 7 d. On d 62, mammary development was scored (0 = no development; 1 = some development; 2 = teat and gland development) by a neutral observer. Treatment with SRE2 increased (P < .05) peak E2 concentrations, duration of luteal function, and mammary gland score. There were no differences (chi-square, P > .05) among doses of SRE2 in the percentage of pseudopregnant gilts that showed luteolysis after PGF2alpha. We conclude that a single injection of SRE2 can induce pseudopregnancy and that the CL can be regressed with PGF2alpha, providing a simple method for controlling estrus in gilts.  (+info)