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During early gestation, hormonal events associated with corpora lutea formation and embryonic synthesis of proteins, prostaglandins, and steroids result in synthesis and release of endometrial secretory products into the uterine lumen. The embryo, inherently and in response to secretory products of the uterus, develops and grows. However, considerable embryonic mortality occurs when uterine secretions become altered in such a manner that they are asynchronous to the developing embryo. Factors that advance or retard development of the uterus and embryo have been utilized to document utero-embryonic asynchrony, and it has been observed that the uterus will not "wait" for embryos to become synchronous. However, the reverse is possible: embryonic development can be accelerated or decelerated. Furthermore within the uterus, localized areas might also exist that favor development of some embryos at the expense of others. This review will consider causes of utero-embryonic asynchrony and offer models of embryonic loss associated with an asynchronous environment in cattle, sheep, and swine.

A single oral dose of mestranol (l7ct-ethynylestradiol 3-methyl ether) was administered to two groups of eight adult female beagle dogs each on Day 6 or 21 after first acceptance of the male. Based on corpora lutea counts, embryonic loss was 95.5 and 67.3%, respectively, for the two treatment groups, and only 34.5% for the control. In a second study a group of 12 beagles were used to determine the effect of mestranol on ova transport. Nine bitches were dosed on Day 6 and the reproductive tracts were removed between 1 and 5 days later and three controls were examined on Day 11. Thirty-nine of a possible 56 ova were flushed from the tracts of the treated females and all but one were from the oviducts. Eighteen (46%) of the ova were degenerating. The controls produced 17 normal zygotes out of a possible 24, and all were flushed from the uteri. Mestranol apparently did not accelerate ova transport, and the possibility of both a direct effect on the ova and an indirect effect via a delay in ova transport is discussed.