Summary. Uterine blood flow and myometrial activity were measured simultaneously in anaesthetized sheep 15 days after a sterile (non-pregnant group) or fertile (pregnant) mating. During the peri-implantation period uterine blood flow was similar in both groups of animals, but spontaneous myometrial activity was greatly reduced in pregnant ewes. This 'block' of myometrial activity was associated with circulating levels of progesterone which were significantly higher (2·8 ± 0·8 ng/ml, mean ± s.e.m.) than those in non-pregnant animals (0·4 ± 0·3 ng/ml). Adenosine injected into the uterine artery produced uterine vasodilatation in both groups, but the log dose–response was significantly less in pregnant than in non-pregnant animals (P < 0·001). Myometrial activity was stimulated by adenosine, particularly in the pregnant group (P < 0·001). Vascular and myometrial effects were potentiated by a previous infusion of dipyridamole. Occlusion of the uterine artery produced reactive hyperaemia, and oestradiol infused close-arterially induced vasodilatation after a lag phase of about 30 min. Our results are consistent with a hypothesis that vascular and myometrial cells in the uterus may contain two types of adenosine receptor, one mediating excitatory and the other inhibitory responses, and that both responses are modified by the presence of a conceptus. The results also support the idea that oestrogens produce uterine vasodilatation by increasing the local concentration of vasoactive substances.

Summary. [³H]Prostaglandin F-2α (PGF-2α) was infused into a uterine lymphatic vessel or a uterine vein for up to 1 h, or injected into the uterine lumen of anaesthetized non-pregnant sheep 7–15 days after oestrus. After an intraluminal injection, labelled PGF-2α was recovered in uterine lymph and peak radioactivity was reached 50 min after injection. [³H]PGF-2α infused at a constant rate into a uterine lymphatic vessel resulted in a maximum concentration of radioactivity in plasma which was 5·6- and 1·7-fold higher in the adjacent utero-ovarian and ovarian vein, respectively, than in carotid arterial plasma. Estimation of the amount of infusate transferred from a lymphatic into ovarian venous blood gave a value (0·4%) similar to that for transfer from a uterine vein (0·3%). Evidence for local transfer was substantiated by the presence of significantly higher concentrations of ³H-labelled compounds in the ovary and corpus luteum adjacent to the site of intra-lymphatic infusion compared with those in the opposite organs. The concentrations in the adjacent ovary and corpus luteum were significantly greater when an intra-lymphatic rather than intra-uterine vein infusion was adopted.

The results show that [3H]PGF-2α is transferred locally from uterine lymphatic vessels into the adjacent ovary, corpus luteum and ovarian vein.

Summary. Lymphatic vessels draining the uterus and ovaries were located within the mesometrium and along the utero-ovarian pedicle by injection of marker dyes into the uterine wall and/or ovary of sheep and goats. Afferent lymphatics drained from the uterus towards the utero-ovarian pedicle and alongside the uterine artery, while 4–12 ovarian lymphatics emerged from the sub-ovarian plexus. A complex lymphatic network was formed in the region of the utero-ovarian pedicle by anastomosis between uterine and ovarian lymphatics. Mixed lymph carried in ducts alongside the uterine artery and in the utero-ovarian pedicle drained into the medial iliac node(s) and lumbo-aortic nodes, respectively. There was no evidence for retrograde lymph flow between the uterus and ovaries, but the close proximity of utero-ovarian lymphatics and the ovarian artery may provide an additional pathway for countercurrent diffusion of prostaglandin F-2α.

Afferent lymph collected after chronic cannulation of utero-ovarian ducts ipsilateral to an ovary bearing a corpus luteum contained a mean progesterone concentration which was 10- to 1000-fold higher than that in jugular vein plasma between 15 and 45 days of gestation. Uterine lymph collected after cannulation of utero-ovarian ducts followed by ipsilateral ovariectomy had a progesterone value equivalent to that in plasma. Protein concentration in utero-ovarian and uterine lymph was between 85 and 90% of that of plasma, while Na concentration was slightly higher, and Cl concentration slightly lower than that of plasma. The concentration of K was similar in both biological fluids, confirming that tissue damage of cannulated vessels was negligible. Cell numbers in utero-ovarian and ovarian lymph were low (200 leucocytes/mm³) and consisted mostly of lymphocytes (>94%). These studies show that leucocytes in lymph are exposed to a high concentration of progesterone, and possibly other related steroids, in the utero-ovarian network which is adjacent to an ovary containing a corpus luteum.

Prostaglandin F_2α (PGF_2α)-induced release of ovarian oxytocin was investigated to determine whether the effect in vivo was local. [³H]PGF_2α infused downstream into a single ovarian lymphatic was transferred into the adjacent ovarian vasculature (estimated transfer 1.1 and 1.7%, two experiments). When unlabelled PGF_2α was infused in a similar manner (76 pmol min⁻¹), there was a prompt eightfold increase in ovarian oxytocin release from the adjacent ovary containing a corpus luteum, but no effect on the opposite corpus luteum, showing that the effect was local. Instillation of 2% lignocaine into the ovarian vascular pedicle did not affect PGF_2α-induced oxytocin release, supporting the idea that neural mechanisms are not involved. Repeated doses of PGF_2α given close-arterially produced a successive reduction in oxytocin release. This effect was prevented by a prior infusion of insulin-like growth factor-I (IGF-I), which itself gave a small, but significant, increase in oxytocin release. The results show that PGF_2α in ovarian lymphatics acts locally and directly to stimulate ovarian oxytocin secretion, that repeated exposure of the corpus luteum to pulses of PGF_2α can result in tachyphylaxis, and that this latter effect can be ameliorated by IGF-I infused in vivo.