J. A. McCRACKEN and B. V. CALDWELL
J. C. CARLSON, B. BARCIKOWSKI and J. A. McCRACKEN
Recent studies suggest that prostaglandins of the E and F series may cause release of the adenohypophysial hormones, ACTH, growth hormone (GH), prolactin and LH. Evidence for the stimulation of ACTH release from the rat pituitary by prostaglandin has been presented by de Wied, Witter, Versteeg & Mulder (1969); Peng, Six & Munson (1970) and Hedge (1972). Hertelendy, Todd, Ehrhart & Blute (1972) observed that intravenous doses (20 μg/kg) of prostaglandin E1 (PGE1) in castrated rams rapidly induced a significant increase in the plasma concentration of GH. Vermouth & Deis (1972) found that two intraperitoneal injections of PGF2α on Day 18 of pregnancy in rats resulted in a biphasic elevation of plasma prolactin at 12 and 20 hr. Indirect evidence exists which indicates that PGF2α may stimulate LH release in the rat (Labhsetwar, 1970; Orczyk & Behrman, 1972; Varavudhi & Chobdieng, 1972).
Systemic infusion of PGF
J C Warning, S A McCracken and J M Morris
Successful pregnancy requires strict temporal regulation of maternal immune function to accommodate the growing fetus. Early implantation is facilitated by inflammatory processes that ensure adequate vascular remodeling and placental invasion. To prevent rejection of the fetus, this inflammation must be curtailed; reproductive immunologists are discovering that this process is orchestrated by the fetal unit and, in particular, the extravillous trophoblast. Soluble and particulate factors produced by the trophoblast regulate maternal immune cells within the decidua, as well as in the periphery. The aim of this review is to discuss the action of recently discovered immunomodulatory factors and mechanisms, and the potential effects of dysregulation of such mechanisms on the maternal immune response that may result in pregnancy loss or preeclampsia.
W. Schramm, H. G. Friesen, H. A. Robertson and J. A. McCracken
Summary. The ability of ovine placental lactogen (oPL) to stimulate progesterone secretion by the ovary as well as its ability to protect the corpus luteum against the luteolytic action of PGF-2α was investigated. When oPL was infused alone into the ovary for 2 h on Day 12 of an induced cycle at rates of 0·6, 6·0, 30·0 or 60·0 μg/h there was no significant increase in progesterone secretion by the autotransplanted ovary in 7 sheep. An extension of the infusion of oPL did not prevent luteal regression during the administration of PGF-2α given either continuously (10 μg/h for 6 h, 5 sheep) or as 5 pulses each lasting 1 h and of increasing concentration in 25 h (2 sheep). We conclude that oPL does not (a) stimulate progesterone secretion when infused directly into the arterial supply of the ovary or (b) have any direct protective effect against the luteolytic action of PGF-2α on the ovine CL.