Glucocorticoids and Estrus in Swine. I. the Relationship between Triamcinolone Acetonide and Estrogen in the Expression of Estrus in Gilts2

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Abstract
Four experiments were conducted to examine the relationship between adrenal corti-coids and estrus in gilts. In the first experiment ovariectomized gilts were given .2, .4, .6 or .8 mg estradiol benzoate (EB) and 0, 2.5, 5 and 10 mg of triamcinolone acetonide (TA), a synthetic glucocorticoid. None of the gilts given .2 mg EB exhibited estrus. Although .4 and .6 mg EB were sufficient to induce estrus, the incidence of estrus was depressed among gilts given .4 mg EB and 5 or 10 mg TA or .6 mg EB and 10 mg TA. The proportion of gilts exhibiting estrus was similar at all levels of TA given in combination with .8 mg EB. In Exp. 2, four gilts given .8 mg EB exhibited estrus while four gilts given .8 mg EB and 20 mg TA did not. The third experiment was conducted in two parts utilizing 26 ovariectomized gilts. The TA was given before EB in part 1 and after EB in part 2. All nine gilts receiving .8 mg EB exhibited estrus. The proportions of gilts exhibiting estrus after receiving .8 mg EB at time 0 and 15 mg TA at -48, -24, -8, 0, 8, 24 and 48 h were 4/5, 5/5, 2/5, 7/10, 1/5, 1/4 and 1/5, respectively. In Exp. 4, intact gilts were given 20 mg TA on d 0, 1, 2 or 3 following an 18 d treatment with allyl trenbolone to synchronize the occurrence of estrus (d 0 = first day compound was not fed). When TA was given on d 2, the proportion of gilts showing a post-treatment estrus was decreased (P<.05). Treatment on d 0, 1 or 3 with TA did not affect the incidence of post-treatment estrus. The frequency of cysts and(or) unovulated follicles was increased (P<.05) by TA treatment (0/6 vs 13/24). These results suggest that TA interacts in a competitive manner with EB to inhibit the expression of estrus. The inhibitory effects in ovariectomized and intact gilts does not appear to be due to decreased adrenal activity caused by TA treatment, but rather to the presence of the synthetic glucocorticoid at a critical time period in the sequence of events leading to estrus and ovulation.

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