Short loop feedback control of the estrogen-induced luteinizing hormone surge in pigs.

Abstract

This study examines whether hCG will block the estradiol-induced LH surge in ovariectomized gilts. Twenty post-puberal cross-bred gilts were ovariectomized at 6-7 months of age. Approximately 2 months later, the experiment was conducted, and all gilts were given estradiol benzoate (EB; 10 micrograms/kg, im) at 0 h. Controls (n = 6) received im saline 24 and 48 h after EB. Two groups of gilts received 2000 IU hCG im, at 24 h (hCG24; n = 5) or 48 h (hCG48; n = 5) after EB. The fourth group (n = 4) received hCG at 48 h and was then given iv a LHRH agonist (des-Gly10, [D-Ala6]LHRH ethylamide) in 100-ng boluses hourly from 54-96 h after EB. Blood samples for determination of LH and FSH were collected every 6 h from 0-96 h. In controls, EB alone suppressed LH from 3.9 +/- 1.9 ng/ml at 0 h to 1.0 +/- 0.2 during 6-48 h (negative feedback), but LH then increased to 4.5 +/- 0.5 between 54 and 96 h (positive feedback), with the peak of the surge (6.7 +/- 1.6) occurring at 72 h. Treatment with hCG did not alter LH during the negative feedback phase (1.1 +/- 0.1 and 1.0 +/- 0.1 for hCG24 and hCG48, respectively). However, there was no LH surge in gilts given hCG at 24 or 48 h (2.4 +/- 0.2 and 2.2 +/- 0.1 form 54-96 h; P less than 0.05). Hourly injections of the LHRH agonist evoked a surge in LH (8.3 +/- 1.3) and maintained elevated LH (4.5 +/- 0.6) between 54 and 96 h, similar (P greater than 0.05) to values for controls. Generally, FSH in gilts given hCG followed the same pattern as LH secretion during the negative feedback stage; however, due to randomization, means for the period from 0-48 h for gilts treated with hCG 24 or 48 h after EB were lower (P less than 0.05) than for controls or gilts given LHRH agonist (62.2 +/- 2.8 and 63.0 +/- 2.7 vs. 79.3 +/- 3.2 and 93.3 +/- 4.2 ng/ml, respectively). During the positive feedback phase (54-96 h), FSH was lower in gilts given hCG (hCG24, 63.4 +/- 2.3; hCG48, 67.3 +/- 2.0) than in controls (86.0 +/- 4.0), but in gilts given LHRH agonist, FSH was higher (1001.1 +/- 7.7) than in controls.(ABSTRACT TRUNCATED AT 400 WORDS)