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Embryonic Dormancy Phenomenon in Obstructed Healthy Mouse Fallopian Tubes

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Abstract

Purpose: A mouse model of unilateral oviductal obstruction was designed to study whether healthy oviducts can support embryo development in an advanced stage toward blastocyst hatching and implantation when the embryos in the contralateral side normally move into the uterine cavity.

Methods: The oviducts of 80 female ICR mice (aged 5–8 weeks) were ligated unilaterally 12–40 hr postcoitus. The ligated oviducts were isolated from day 4 to 19.5 postcoitus. Embryos within the ligated oviducts were then flushed out to record the developmental stage and compared with the conceptuses in the contralateral uterine horns with unligated oviducts. Embryos recovered from ligated oviducts were then cultured in vitro to observe their potential for further development.

Results: In 33 mice, 53.4% (163/305) and 86.1% (241/280) of the morphologically normal blastocysts had hatched from the zona pellucida within the obstructed tube and contralateral uterine horns, respectively, on the 5th day postcoitus. The data demonstrated that the hatching process could take place within the obstructed fallopian tube, but the timing was delayed. From 5.5 to 19.5 days postcoitus, a total of 362 implanted embryos were obtained in unligated control uterine horns, but none of the 404 embryos in the artificially obstructed oviducts were implanted. The embryos within the ligated tubes were dormant in the hatched blastocyst stage as demonstrated by their ability to continue growing (98.2%) when removed from the oviduct to an in vitro environment.

Conclusions: In this study, we demonstrate that mouse embryos can hatch, although delayed, in obstructed healthy oviducts. Tubal pregnancy is not likely to happen in artificially obstructed healthy mouse fallopian tubes, since all the viable embryos were dormant at the hatched blastocyst stage.

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Lee, R.KK., Lin, SP., Tsai, YJ. et al. Embryonic Dormancy Phenomenon in Obstructed Healthy Mouse Fallopian Tubes. J Assist Reprod Genet 17, 540–545 (2000). https://doi.org/10.1023/A:1009402126770

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  • DOI: https://doi.org/10.1023/A:1009402126770

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