Intrauterine Migration of the Porcine Embryo: Influence of Estradiol-17β and Histamine

Abstract

The role of estradiol-17 beta (E2) in migration of the porcine embryo was examined (Experiment 1) by observing the distribution of Silastic (polydimethyl siloxane, Medical Adhesive Silicone Type A, Dow Corning) beads impregnated with cholesterol or E2 (n=5 gilts per treatment) after 5 days in utero (Day 12 of the estrous cycle, Day 0=1st day of estrus). Beads impregnated with E2 migrated farther (P less than 0.05) than those impregnated with cholesterol. Twenty additional gilts and sows were used to determine if histamine was involved with intrauterine migration (Experiment 2). On Day 6 of gestation the tip of each uterine horn was exposed and the subserosa of each of 5 gilts was injected with either vehicle, 8 mg of cromolyn sodium (an inhibitor of histamine release) or 8 mg of cromolyn sodium plus 1 mg of histamine. Four days later (Day 10), the excised uterus was examined for migration of embryos. An additional group of 5 gilts received 8 mg of cromolyn sodium on Days 6 and 10 and were examined on Day 12. Results from the second experiment demonstrated that cromolyn sodium treatment alone restricted (P less than 0.05) Day 10 embryos to the tip of the uterine horn but by Day 12 embryos had overcome this restriction. Injection of histamine overcame the inhibitory effects of cromolyn sodium and restored migration of Day 10 embryos. These experiments suggest that both E2 and histamine are involved in intrauterine migration of the porcine embryo. The extent to which these hormones might be interrelated during migration is not fully understood at this time.

Developmental arrest of scNT‐derived fetuses by disruption of the developing endometrial gland as a result of impaired trophoblast migration and invasiveness

“…However, analysis of 12 scNT-derived placentas revealed that all fetuses had severe placental abnormality. An early pregnancy loss or first-trimester miscarriage in the control is the most common complication in pig reproduction, with an incidence range between 20 and 30% of all conceptions, and another 10-15% loss occurs at midgestation (Pope et al, 1982;Stroband et al, 1990;Pope, 1994). Embryonic loss can be derived from the embryo and/or the uterine environment.…”

“…Early embryonic mortality occurs in high frequency during a period of gestation known as the embryonic period: 20-30% of pig fetuses die between gestational day 12 and 30, and another 10-15% loss occurs at midgestation (Geisert et al, 1982;Pope et al, 1982;Pope and First, 1985;Stroband and Van der Lende, 1990;Pope, 1994;Geisert and Schmitt, 2001). The factors implicated as the causes of early embryonic mortality can be broadly categorized as intrinsic (endometritis and periglandular fibrosis) (Parker et al, 2004;Inagaki et al, 2005), extrinsic (environmental or management-related factors, such as stress, poor nutrition, and body condition) (Lucy, 2001;Eugster et al, 2004;Campagne, 2006), or embryonic factors (Geisert et al, 1982;Pope and First, 1985;Geisert and Yelich, 1997).…”

Estrogen metabolism by the equine embryo proper during the fourth week of pregnancy

“…Although the full significance of this synthesis has not yet been established, it is presumed that estrogens play a role in the maintenance of pregnancy. A similar situation occurs in early pregnancy in the pig, where estrogen synthesis by the blastocyst is seen around days 10-12 of pregnancy (Perry et al 1973), a time when 17b-estradiol (E 2 ) has been shown to influence intrauterine migration of embryos (Pope et al 1982) and uterine prostaglandin F 2a secretion (Bazer & Thatcher 1977). Estrogen formation by the early pig embryo is limited in duration with a transient expression of cytochrome P450 aromatase (P450 arom ) enzyme in the trophoblast, between days 10 and 12 (Conley et al 1992(Conley et al , 1994.…”

Production of Steroids and Release of Prostaglandins by Spherical Pig Blastocysts in vitro

“…Blastocyst-derived oestrogens could participate in early porcine pregnancy by initiating blastocyst spacing (Pope et al 1982), stimulating endometrial secretion (Geisert et al 1982b), promoting luteal maintenance (Gardner et al 1963;Ford and Magness 1980) or by stimulating uterine blood-flow (Dickson et al 1969;Ford et al 1982). By regulating calcium flux in endometrial cells, oestrogens of conceptus origin (Fishel 1979) could also activate phospholipase and thereby enhance local PG synthesis (Rubin and Laychock 1978).…”