Influence of oophorectomy, luteectomy, foetal death and dexamethasone on the peripheral plasma levels of oestrogens and progesterone in the pregnant Macaca mulatta.
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Biomedical subjects
Publications and source records attributed to W T Bosu.
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Three groups of ovariectomized Holstein heifers were used in this study. Group I heifers (n = 6) were pretreated with saline (SAL), followed 3 h later by three injections of naloxone hydrochloride (NLX) given 1 h apart. In the same sequence, group II heifers (n = 3) received lipopolysaccharide (LPS), followed by the opioid antagonist NLX. Group III heifers (n = 3) received LPS followed by SAL. Concentrations of cortisol and progesterone increased (P < 0.05) following LPS injections in both groups II and III, whereas luteinizing hormone (LH) concentrations were suppressed (P < 0.05). Administration of NLX to heifers pretreated with LPS elicited significant increases (P < 0.05) in LH concentrations, whereas SAL infusion had no effect. These results indicate that the inhibitory actions of opiate mu-delta receptors, and possibly other POMC gene products, were at least partially involved in LPS-induced suppression of the gonadotropic hormone. These results are discussed, including the possibility that feedback suppression by LPS-triggered adrenal gland steroids may have interfered with complete restoration of LH secretion by the opioid antagonist.
The effects of high systemic concentrations of ACTH during the days preceding ovulation on follicular wall and luteal tissue LH receptor concentration were studied at the expected time of ovulation and their evolution thereafter in 12 ewes. Controls (C; n = 3), received ten injections of sterile saline every 12 h, on days 11-16 of the estrous cycle, treated ewes (T1, T2, T3; three animals each) received ten injections of ACTH (50 IU every 12 h). Ovariectomies were carried out in C and T1 on day 16, in T2 on day 18 and in T3 on day 21. Relative to C, follicular concentration of LH receptors was approximately 50% in T1 ewes (P < 0.025); but slightly higher (62%) in T2, and dramatically increased (167%) in T3. None of the animals displayed a preovulatory LH surge. ACTH treatment induced significant pathological effects on ovarian structures probably through treatment-induced increase in cortisol.