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Weight of placental tissues of cows increased exponentially from Day 100 to Day 250 of gestation, but at much slower relative and absolute rates than fetal weight. In addition, growth rate of fetal placental tissues was less than that of maternal placental tissues. Concentrations of DNA, RNA and protein, however, increased in fetal placental but not in maternal placental tissues. Fetal placental tissues therefore exhibited hyperplasia, which probably contributes to increased functional capacity of the placenta during late gestation. The rate of O2 uptake in vitro was greatest for maternal placental tissues, suggesting that the maternal portion of the placenta accounts for most of the large rate of placental O2 utilization in vivo. Compared with other placental tissues, rate of secretion of macromolecules by intercaruncular endometrium was high, but decreased from Day 100 to 250, suggesting that uterine glandular secretory activity may decrease as gestation advances. Rate of secretion of macromolecules also was high for intercotyledonary tissues and increased with day of gestation, suggesting a role for secretory products of chorioallantois in gravid uterine function.

Samples from corpus haemorrhagicum, mid-cycle corpus luteum (CL) and late-cycle CL were tested for their abilities to stimulate neovascularization of chorioallantoic membranes (CAM) of developing chicks. Responses were graded from 0 to 4 (4 being the greatest response). Luteal tissue implants from each stage of the oestrous cycle stimulated growth of CAM blood vessels, and vascular responses increased with age of CL. Implants from late-cycle CL were typically graded 3 or 4. Luteal tissues from several stages of development were also incubated for 6 h in serum-free medium containing no hormone, LH, PGF-2 alpha or both hormones. Media conditioned by luteal tissues were assayed for progesterone and tested for their ability to stimulate mitogenesis and migration of bovine aortic endothelial cells in vitro. All media conditioned by luteal tissues stimulated mitogenesis and migration of endothelial cells, but media from late-cycle CL exhibited the greatest activity. Luteinizing hormone significantly increased in-vitro secretion of a factor(s) that stimulated migration of endothelial cells. PGF-2 alpha alone had no effect on production of endothelial cell mitogen or migration-stimulating factor(s) from luteal incubations; however, the ability of LH to enhance secretion of the migration-stimulating factor(s) was blocked by PGF-2 alpha. This study demonstrates that angiogenic activity of bovine luteal tissues increases with age of the CL and in-vitro secretion of angiogenic factor is responsive to hormones known to regulate luteal function.

In Study 1, explants of caruncular and intercaruncular endometrium and fetal membrane were collected from ewes (5-6/day) on Days 11-13, 16-18 and 21-23 after mating and Days 10-12 after oestrus, and incubated for 24 h. Explant-conditioned media were evaluated for their effects on endothelial cell proliferation. Both caruncular and intercaruncular endometrium secreted factor(s) which stimulated endothelial cell proliferation, and which appeared to be greater than 100 x 10(3) Mr and heat-labile. In Study 2, conditioned media from explant incubations of caruncular and intercaruncular endometrium, cotyledon and intercotyledonary fetal membrane obtained from ewes (6-7/day) on Days 40, 65, 90, 115 and 140 after mating were evaluated for their effects on endothelial cell proliferation. Caruncular and intercaruncular endometrium and intercotyledonary fetal membrane secreted factor(s) which inhibited endothelial cell proliferation. Media from cotyledonary explants tended to stimulate endothelial cell proliferation on Day 115. Conditioned media from cotyledonary explants obtained from 3 additional ewes at Day 120 of gestation stimulated endothelial cell proliferation, and this activity also appeared to be greater than 100 x 10(3) Mr. Placental angiogenesis in ewes therefore appears to be modulated by both maternal and fetal placental tissues via stimulatory and inhibitory factors.

In Exp. 1, maternal (caruncle) and fetal (cotyledon) portions of the placenta as well as uterine endometrium were obtained from cows at mid-gestation and evaluated for angiogenic activity by placing tissue samples on chick chorioallantoic membranes (CAM). Only caruncular tissues exhibited angiogenic activity in the CAM assay. In Exp. 2, lyophilized homogenates of caruncular tissues obtained from cows at mid-gestation were evaluated for angiogenic activity on CAM and for their ability to stimulate mitosis of bovine aortic endothelial cells in vitro. Homogenates of caruncular tissues again were angiogenic on the CAM and also were mitogenic for endothelial cells. In Exp. 3, maternal (caruncle and endometrium) and fetal (cotyledon and fetal membrane) portions of the placenta were obtained from cows at mid-gestation and fine minces (explants) of each were cultured for 24 h. Explant-conditioned media were then tested for angiogenic activity by their abilities to stimulate mitosis and migration of bovine aortic endothelial cells in vitro. Conditioned media from caruncular explants, but not from explants of other tissues, exhibited both mitogenic and migration-stimulating activities. When pools of caruncular explant-conditioned media were fractionated by ultrafiltration, mitogenic activity was not present in fractions of Mr less than 10,000, less than 30,000 and less than 100,000, but was retained in fractions of Mr greater than 10,000, greater than 30,000 and greater than 100,000. Mitogenic activity was not observed in any fractions subjected to heat treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

In conjunction with the tremendous physiological changes that occur in the corpus luteum (CL) during the estrous cycle are equally dynamic intrinsic vascular changes (Bassett, 1943). Since the CL receives one of the greatest rates of blood flow of any organ (Bruce and Moore, 1976; Ford et al., 1982), factors that regulate luteal angiogenic processes may be important determinants of subsequent luteal function.