Early embryonic survival in the pig: Can it be improved?

ABSTRACT A major limitation for increasing litter size in swine is embryonic loss that occurs during the 2nd to 3rd wk of gestation. High ovulation rates of modern sows have more than supplied the potential number of embryos necessary to improve litter size. The current challenge is determining how early conceptus development affects the ability to maintain the viability through the remaining 90 d of gestation to maximize farrowing house production. To achieve this, it is necessary to identify and understand the possible causes of embryonic death. Because fertilization rates are generally high in swine, early embryonic loss during the first 20 d of gestation is considered to critically effect potential litter size. There are three periods during which early embryonic loss can occur: 1) pre-elongation development, 2) trophoblastic elongation, and 3) placental attachment. The first two periods are related to time of fertilization and subsequent developmental rate for each individual embryo within the litter. Asynchrony in embryonic development relative to uterine development can result in loss of embryos before d 10 of gestation. Competitive acquisition of adequate uterine space between littermate embryos, essential for blood flow delivery of nutrients needed for survival to term, is established during conceptus elongation on d 12 of gestation. Progressive changes in the uterine microenvironment between d 10 and 16 of gestation play a major role in embryonic survival following trophoblast elongation and placental attachment. In current production systems, there can still be sufficient numbers of embryos present after d 30 of gestation to provide improvement in average litter size at farrowing. However, producers are still faced with the challenge of maximizing fetal survival to term. Therefore, fully understanding the biological controls of follicle ovulation rate, synchrony of ovulation, embryonic developmental rate, uniformity of conceptus elongation, uterine horn capacity, uterine glandular and vascular development, and placental vascularization could provide possible clues to improving embryo quality.

Implications

The numerous biological factors involved with regulating litter size in pigs have slowed progress for rapidly increasing litter size. Our knowledge of the factors regulating conceptus and uterine development and function has increased but is far from complete. The developing technologies to investigate gene and protein expression will continue to assist in unraveling the mysteries of early embryonic survival in the pig. However, improvements in litter size will only occur when we can use the information to increase placental efficiency and(or) uterine secretory function. It is clear that the uterus in the pig can be modified to alter glandular development. Therefore, a combination of increased endometrial glandular density and placental vascularity may move litter size beyond the current plateau currently achieved in the swine industry.

Key Words: Embryo, Pigs, Pregnancy, Uterus

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J. Anim. Sci. 80(E. Suppl. 1):E54-E65