Ovarian Function and Early Embryo Development in Immature Rats Given a Superovulatory Dose of PMSG, Later Neutralized by Antiserum1
- 1 September 1981
- journal article
- research article
- Published by Oxford University Press (OUP) in Biology of Reproduction
- Vol. 25 (2) , 272-280
- https://doi.org/10.1095/biolreprod25.2.272
Abstract
Use of exogenous gonadotropin to induce ovulation may be associated with reduced fertility resulting from excessive follicular stimulation. To investigate this problem further a superovulatory dose of 40 IU PMSG [pregnant mare serum gonadotropin] was administered to 29-day-old rats at 0800-0900 h on day -2 of the experiment (SOV animals). Control rats received 4 IU PMSG, a dose which induces a physiological number of ovulations followed by a normal pregnancy. A volume of antiserum (a/s) known to inhibit completely the ovarian and uterine weight increasing capacity of 40 IU PMSG was injected i.p. at 1800 h on day 0 to 50% of the SOV group (SOV a/s animals). Females were then caged with mature fertile males overnight, examined for evidence of mating on day 1, and sacrificed at 1030-1230 h on days 1-5. Tissue and blood were collected for steroid analyses, and oviducts and uteri were flushed to determine the number and location of embryos. Animals receiving a/s had higher embryo recovery on days 4 and 5 compared with SOV animals. On day 5 a mean of 10.5 embryos was recovered from SOV a/s animals compared with 8.2 in control rats and 2.4 in SOV animals. On day 5 most SOV animals had no embryos; following a/s all animals were pregnant and the majority of embryos were in the uterus. In control rats all embryos were in the uterus on day 5. Serum and ovarian progesterone levels were 3- to 4-fold higher in SOV animals compared with controls, but were unchanged by a/s administration, estradiol-17.beta. in both serum and ovaries was drastically reduced to levels close to those observed in control rats within 18 h of a/s administration. Early embryo loss after superovulation may result, at least in part, from excessive estrogen secretion, probably arising from remaining follicles. This loss could occur through stimulation of either the oviductal or uterine environments or both.This publication has 13 references indexed in Scilit:
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