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Results for “Ovulation Induction”

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PubMed1978

Effect of melatonin on induction of ovulation in the light- induced constant estrous-anovulatory syndrome and possible role of the brain serotoninergic system.

Continuous light (CL) induces constant estrous anovulatory (CEA) syndrome and blockade of pineal gland activity. Chronic treatment with metatonin is able to overcome the anovulatory state in about 70% of CL-CEA rats, and the luteinizing effect of melatonin is significantly counteracted either by feeding the animals with a tryptophan-poor diet or by injecting methiothepin, a blocker of central serotoninergic receptors. It appears that melatonin elicits luteinization in CL-CEA rats through the brain serotoninergic system.

Animals↗
PubMed1975

Induction of ovulation in infertile women with pituitary tumors.

Four infertile women with pituitary adenoma were treated with human pituitary gonadotropins (HPG) in order to enable them to become pregnant. During pregnancy they contracted headache, bitemporal visual field defects, or impaired visual acuity. One woman was operated upon in the second trimester; the other three, as the symptoms were relatively moderate and no risk of permanent damage to the optic tract existed, went to term. After operation or delivery the symptoms disappeared.

Adenoma↗
PubMed1985

Evidence for a positive feedback interaction between progesterone and luteinizing hormone in the induction of ovulation in the hen, Gallus domesticus.

Two experiments were conducted to test the hypothesis that progesterone (P4) acts to induce a preovulatory rise of luteinizing hormone (LH) by initiating a true positive feedback interaction between P4 and LH. In each experiment, ten hens were stereotaxically implanted with a third ventricle cannula. Aminoglutethimide phosphate (AGP), an inhibitor of steroidogenesis, was administered (200 mg iv) to hens at 10 and 6 hr (Experiment 1) and 10 and 7 hr (Experiment 2) before an expected C1 ovulation. A 20-micrograms injection of P4 (n = 5) or the vehicle (n = 5) was made intraventricularly at 6 hr (Experiment 1) or 7 hr (Experiment 2) before the expected ovulation. Blood samples were taken via branchial vein cannula at regular intervals after the injection. In Experiment 1, four of five P4-treated hens ovulated, and no atretic follicles were found in any of the five P4-treated hens, including the one which did not ovulate. Ovulations were always accompanied by preovulatory LH peaks. By comparison, none of the vehicle-injected animals ovulated and in four of five hens the largest follicle was determined to be atretic. No ovulations occurred in Experiment 2 for either the P4- or vehicle-injected hens. Atresia of the largest follicle occurred in all five hens in the P4-treated group and four of five hens of the vehicle-treated group. The difference in results between Experiment 1 and Experiment 2 can be explained assuming that the steroidogenesis-inhibiting action of the initial AGP injection in Experiment 1 (at 10 hr before ovulation) had diminished prior to the second AGP treatment (at 6 h before ovulation).(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoglutethimide↗
PubMed1988

Induction of ovulation and oviposition in female quail with luteinizing hormone, luteinizing hormone releasing hormone, or progesterone.

Regularly laying female Japanese quail were injected 12 or 18 hr before the next expected oviposition with 25 micrograms oLH, 25 micrograms luteinizing hormone releasing hormone (LHRH), or 0.05 mg progesterone, and the subsequent oviposition was recorded and ovulation determined by autopsy 9 hr after the injection. Plasma progesterone levels were measured in blood collected from a wing vein during the postinjection interval. Vehicle-injected birds served as control. All treatments resulted in premature oviposition and ovulations in 50-100% of birds when injected 12 hr before the next expected oviposition. None of the vehicle-injected birds showed any advancement in either oviposition or ovulation. Premature oviposition was generally followed by premature ovulation within 1 hr, when birds were treated 12 hr before the next expected oviposition and was preceded by a rise in plasma progesterone levels which reached values similar to those occurring during the normal preovulatory period. When birds were injected 18 hr before the next expected oviposition, the incidence of premature oviposition was very low, premature ovulation was absent, and the rise in plasma progesterone levels following treatment was substantially less than in the former group. The results suggest that oviposition and ovulation in quail may be initiated by LHRH induced LH release from the pituitary gland and that progesterone may stimulate LHRH and LH release. The timing of the ovulatory cycle may depend upon the phase of follicular maturation.

Animals↗