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P. V. HOLMES and S. BERGSTRÖM

Summary.

Oestrogen administration to female mice with `delayed' implantation induces changes in the uterus and blastocysts followed by implantation and normal gestation. The second messenger for oestrogen, adenosine 3′:5′-cyclic monophosphate (cAMP), was instilled into the uterine lumen of females with `delayed implanting' blastocysts to determine whether it also is able to induce implantation. Implantation of the blastocysts was induced by cAMP but the pregnancies were not maintained to term. These results are discussed with respect to the changes in blastocysts induced by cAMP and with respect to the reported contraceptive effects of cAMP in normal mice.

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P. V. HOLMES and A. D. DICKSON

Summary.

A secretion from mouse trophoblast was investigated using the mouse adrenal X-zone, which degenerates differently under the influence of androgens and progestagens. Blastocysts were transplanted under the kidney capsules of female mice and, subsequently, the kidneys and adrenals were examined histologically for trophoblast growth and X-zone degeneration, respectively. Adrenal X-zone degeneration was evident in immature mice only when they received blastocyst transplants, correlating trophoblast proliferation with X-zone degeneration. The degeneration found in both transplanted and control adults correlates maturity with X-zone regression. The fact that the mode of degeneration was always histologically similar to that induced by progestagens implies a progestagenic mediation.

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P. V. Holmes, J. Sogn, E. Schillinger and P. O. Janson

Summary. Rabbit ovaries were isolated surgically before the ovulatory gonadotrophin stimulation and perfused in vitro. Untreated, control ovaries never ovulated. Ovaries treated in vitro with ovine LH ovulated 10–14 h later and the oocytes had undergone germinal vesicle breakdown (GVB). LH induced increases in progesterone secretion from the treated ovaries. A 3β-hydroxysteroid dehydrogenase blocker ('Compound A') effectively reduced progesterone secretion into the perfusate and follicular fluid to very low levels but had no effect on ovulation rate or on oocyte maturation. Excessively high progesterone levels were obtained artificially in perfusates by addition of exogenous steroid; the number of ovaries ovulating was markedly reduced but there was no effect on oocyte maturation.

It is concluded that the rise in progesterone that normally occurs immediately after the LH surge is not a prerequisite for ovulation in the rabbit. However, progesterone may have a modifying effect on LH-induced follicle rupture when at a pharmacologically high level.

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B. M. Mutayoba, P. D. Eckersall, I. A. Jeffcoate, V. Cestnik and P. H. Holmes

Changes in pulsatile secretion of LH and testosterone and responses to exogenous GnRH were assessed at different stages of Trypanosoma congolense infection in rams. Jugular blood samples were collected every 15 min for 6 h followed by immediate injection of GnRH (20 μg i.v.) and further sample collection after 10, 20, 40, 60, 80, 100 and 120 min. This sampling and injection regimen was performed 5 days before infection (day − 5) and 23 and 52 days after infection. T. congolense infection increased (P<0.05) the mean plasma LH concentration over 6 h on day 23 (3.2 ± 0.2 ng ml−1) and decreased (P < 0.05) the mean LH concentration on day 52 (1.2 ± 0.2 ng ml−1, P < 0.05) compared with day − 5 values (2.0 ± 0.2 ng ml−1). Trypanosome infection induced a rapid decline in plasma testosterone concentration from a mean of 7.5 ± 1.4 nmol l−1 on day − 5 over 6 h to 3.6 ± 0.4 nmol l−1 (P<0.05) on day 23 and 1.7 ±0.3 nmol l−1 (P< 0.001) on day 52. The observed decline in plasma LH concentration in infected rams was not associated with reduced sensitivity of the pituitary to GnRH or its ability to release LH, as the LH response to exogenous GnRH was not impaired throughout the period of infection. However, the testosterone response to GnRH-induced LH stimulation was depressed on both days 23 and 52 after infection. It was concluded that the decline in plasma LH concentration in infected rams was caused by reduced GnRH stimulation of the pituitary, whereas the decline in plasma testosterone was partly caused by reduced sensitivity of the Leydig cells to circulating LH.