Influence of anaesthetics, mating, premature delivery, the time of day of blood sampling, and suckling on plasma levels of luteinizing hormone in hamsters.

The influence of several factors on immunoreactive LH levels in peripheral plasma of female hamsters was investigated. The LH values for animals anaesthetized with either sodium pentobarbitone or chloral hydrate were significantly lower (P smaller than 0-01) than those values obtained for hamsters sampled under ether anaesthesia. Mating on the night of pro-oestrus resulted in increased LH levels (P smaller 0-01) the following morning as compared with the levels in control females not caged with males. The LH levels were relatively low (13 plus or minus 2 (S.E.M.) ng/ml) on the afternoon (16.00-18.00 h) of day 15 of pregnancy and also on the morning (09.00-10.00 h) of day 16 before (7 plus or minus 1 ng/ml) and after parturition (4 plus or minus 0-2 ng/ml), but rose severalfold (561 plus or minus 201 ng/ml) on the afternoon post partum. When premature delivery was induced on day 15 of pregnancy by administration of prostaglandin E2 the LH levels did not rise on the afternoon of this day (29 plus or minus 11 ng/ml), but did so on the following afternoon (213 plus or minus 115 ng/ml), at the same interval post coitum as in normal delivery. Marked increases in the concentration of LH in plasma were observed on the afternoon of each of days 0-6 post partum. The levels were comparable to those found on the afternoon of pro-oestrus in cyclic hamsters and could be blocked by administration of sodium phenobarbitone at 13.00 h. Similar afternoon surges of LH were not observed during dioestrus. In the morning, the LH levels were significantly higher (P smaller 0-001) in the non-suckled dams (95 plus or minus 4 ng/ml) than those in mothers allowed to nurse their young (13 plus or minus 4 ng/ml). In contrast, the levels in the afternoon were unaffected by the suckling stimulus (suckled, 495 plus or minus 76 v. non-suckled, 744 plus or minus 165 ng/ml; P greater than 0-05).

Progesterone: sites of action in inhibiting ovulation in hamsters.

A single subcutaneous injection of progesterone (0.5 mg/animal at 17.00 hours) on Day 3 of the cycle (Day 1 = day of vaginal discharge) interfered with ovulation and external vaginal discharge in all the animals. Lower doses were only partly active. Intravenous administration of LH, FSH or their combination at 14.00 hours on Day 4 failed to restore ovulation in such animals, implying a direct action of the administered progesterone on the ovary. A large dose of oestradiol benzoate (400 mug/animal) also proved inactive suggesting that progesterone did not interfere with ovulation solely through antioestrogenic action. Depletion of the pituitary LH stores normally found in association with ovulation and ovulatory peak of LH in plasma seen in control animals were not observed in the progesterone-treated hamsters suggesting a further action of progesterone at the pituitary-hypothalamic level in inhibiting ovulation. Administration of synthetic LRF (100 ng/animal, i.v.) on Day 4 to hamsters treated with progesterone caused an increase in plasma LH 15 min later which was comparable to the rise observed in control animals given a similar injection of LH-RF, implying lack of action of progesterone at the pituitary level. It is concluded that progesterone acts centrally, principally on the hypothalamus, and peripherally on the ovary to interfere with ovulation in hamsters. It is possible that the anovulatory state accompanying pregnancy results from these actions.

Letter: Prostaglandins and catecholamines in gonadotropin secretion.

PIP: The hypothesized role of PGF in potentiating adrenergic transmission, known to be involved in gonadotropin secretion, was tested in McCormack-Mayer model involving use of 26-day old immature rats primed with 5 iu of PMS and given a single subcutaneous injection of progesterone 24 hours later. Aspirin was injected into the 3rd ventricle prior to the onset of the critical period on the day of the progesterone injection. Bilateral injections of aspirin into the anterior hypothalamic area (AHA) during onset of critical period were found to block the facilitatory effect of progesterone. Simultaneous injection of PGF2a or dopamine into AHA however fully restored ovulation blocked by aspirin. The results show that prostaglandins and catecholamines (CA) interact to induce adrenergic transmission normally required for gonadotropin secretion. The study also demonstrates the failure of aspirin in the dose used (60 to 100 mcg) to suppress prostaglandin synthesis in the relevant area of the hypothalamus, e.g., AHA, where CA fibers are known to most likely form synapses with LRF secreting neurons. This finding partly explains the failure of peripherally administered indomethacin to affect LH secretion in Patrono and Serra's experiment. Other studies cited suggest possible role of hypothalamic and/or pituitary prostaglandins in gonadotropin secretion. Subcutaneous administration of indomethacin may be more effective in inhibiting prostaglandin synthesis in the ovary than in the hypothalamus, possibly due to differential sensitivity of these tissues and/or poor penetration of the drug across the blood-brain barrier.^ieng