Luteolytic Effect of LH and HCG on the Corpora Lute a of Pseudopregnant Rabbits1
- 1 January 1966
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 78 (1) , 67-74
- https://doi.org/10.1210/endo-78-1-67
Abstract
Corpora lutea induced in 133 estrous rabbits by HCG (human chorionie gonadotropin) were marked for future identification by India ink injection into each corpus luteum 2-4 days post ovulation. In Exp. I, a 2nd set of corpora lutea was induced with HCG on days 3-13, all of which were maintained for 17-20 days after ovulation. The initial set of corpora lutea was maintained for the full life of the secondary set following HCG on day 3, and partially maintained after HCG on day 4, but regressed rapidly following injection of HCG after day 5. In Exp. II, FSH (follicle-stimulating hormone) and LH (luteinizing hormone) singly or in combination were used to induce a 2nd group of corpora lutea on day 7. FSH alone provoked regression in some, but not all, of the marked initial corpora lutea. FSH and LH or LH alone caused rapid regression of the initially formed corpora lutea, while the 2nd group of corpora lutea persisted for a normal 17-18 day period. In Exp. III, 1.0 mg estrone sc daily on days 5-8, superimposed on HCG on day 7, prevented immediate regression of the initial corpora lutea and allowed their persistence for 17-18 days. Day 7 HCG-induced corpora lutea also had a 17-18 day life span. Thus, initial and secondarily induced corpora lutea regressed asynchronously. In Exp. IV, exogenous LH, started on day 7 of pseudopregnancy and 5-7 hr. post hypophysectomy, failed to maintain the initial corpora lutea. The initial corpora lutea rapidly regressed as in intact LH-treated rabbits. In Exp. V, HCG caused rapid regression of the initial corpora lutea in hysterectomized, pseudopregnant does when given on day 7 or 13 of pseudopregnancy, but it had no luteolytic effect when given on day 3. HCG or LH in the pseudopregnant doe may have caused corpora lutea regression by interfering with endogenous estrogen via a direct effect on the ovary.This publication has 0 references indexed in Scilit: