Summary. The effects of isolated protein fractions from rabbit uteri (prealbumin, albumin, uteroglobin, and \g=b\-glycoprotein),unfractionated uterine proteins, progesterone, oestradiol-17\g=b\, and prostaglandin F-2\g=a\on the development of rabbit embryos in vitro were investigated. When exposed to individual protein fractions obtained from Day-6 uteri, 8-cell embryos did not develop into early blastocysts; morulae readily developed into early blastocysts, but further development was retarded. Progesterone (10\ p=n-\ 5\ p=n-\ 10\ p=n-\ 11m) and prostaglandin F-2\g=a\(0\m=.\1\p=n-\10 ng/ml) added to the medium slowed development of blastocysts to advanced stages. Growth of 8-to 16-cell embryos, morulae, and Day-4 blastocysts was stimulated by unfractionated uterine proteins obtained from Day-5 uterine flushings.Although embryos cultured in medium containing BSA had similar rates of blastocyst formation and, ultimately, similar blastocyst expansion as did the embryos cultured in medium with unfractionated proteins, the radial and immediate expansion of the early blastocysts cultured in the latter approximated that found in utero.

One hundred and two nonparous females, 18 to 24 mo old, and 55 parous or multiparous beef females, 3 to 12 yr old, were mated naturally (d 0) and slaughtered on d 2 to 5, 6 to 8 or 14 to 16 of gestation. Each reproductive tract was flushed with phosphate-buffered saline, and the flushings were searched for an oocyte or embryo. Parous females had a higher (P less than .05) fertilization rate than nonparous females. In nonparous females, reproductive failure was attributed equally to fertilization failure and embryonic mortality, which had occurred or was occurring by d 8 of gestation. In parous females, reproductive failure was attributed entirely to embryonic death. About 67% of this embryonic mortality had occurred or was occurring by d 8 of gestation; the other 33% occurred between d 8 and 16 of gestation. These findings show that in both nonparous and parous beef females, a large portion of the reproductive failure occurs by d 8 of gestation and would not have any noticeable influence on length of the estrous cycle.

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.

Straightbred and crossbred heifers (165) and cows (241) that were nonpregnant after exposure to fertile bulls for two consecutive breeding periods of 45 to 60 d (repeat breeders) and contemporary cows (102) that had produced a calf in the previous calving season (controls) were placed with bulls and were observed for mating. Repeat-breeder and control females were slaughtered at 2 to 51 d postmating. Data were accumulated over 4 yr. From previous calving records, repeat breeders had more (P<.05) calving difficulty than controls. Percentages of females with anatomical aberrations or anovulation were 10.9 and 3.6, and 0 and 2.9, respectively, for repeatbreeder and control females. Repeat breeders had fewer (P<.01) normal embryos and higher (P<.01) nonreeovery rates of an embryo or oocyte than controls. Precentages of normal, degenerate, unfertilized, or nonrecoveries were 42.3, 8.9, 8.0 and 40.8, and 76.8, 9.1, 6.0 and 8.1 for repeat breeders and controls, respectively. Repeat breeders had fewer (P<.01) 1-to 3-ram follicles than controls (25.4 and 36.5, respectively). On d 6 postmating, controls had higher (P<.O1) serum progesterone concentrations than repeat-breeders (2.7 vs 1.8 ng/ml, respectively). Chromosome aberrations were found in lymphocytes of 19 of 133 (14.3%) repeat-breeders. Increased anatomical aberrations of the reproductive tract, increased anovulations, lower recovery rate of an oocyte or embryo, lower progesterone concentrations at d 6, fewer 1-to 3~mm follicles and increased chromosomal abnormatilities are possible causes for lower fertility in repeat-breeder females.

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Samples of uterine horn, broad ligament (mesosalpinx and mesometrium), and uterine artery of ten unilaterally ovulating cows, 12-15 days after mating, were examined for differences in concentration of progesterone. Tissues (mesosalpinx, branches of the uterine artery, anterior uterine horn) adjacent to the ovary bearing the corpus luteum contained significantly greater quantities of progesterone than more distal tissues (mesometrium, uterine artery, posterior uterine horn) on the same side and all tissues on the contralateral side. In tissues on the side ipsilateral to the corpus luteum, a gradient of progesterone existed. Differences in tissue concentrations of progesterone may be the cause of observed differences in uterine physiology in the cow and ewe.