ABSTRACT. Reproductive diseases after parturition are a serious problem in dairy cattle. It is important to predict postpartum reproducti ve diseases early and to develop prophylaxis. The objectives of this study were to demonstrate changes in the peripheral blood con centration of interleukin-6 (IL-6) before parturition, which was mainly produced by T helper 2 type (Th2) cells, and to investigate a correlation between the IL-6 concentration and the occurrence of the postpartum retained placenta, endometritis and/or follicular cyst in da iry cattle. Twenty-seven Holstein-Friesian cows were used for this study. Thirteen had no clinical disease, 8 had retained placenta, 4 were diagnosed with endometritis by vaginal inspection, and 2 were diagnosed with follicular cyst by rectal palpation at 1 and 2 months a fter parturition. Blood samples were collected 60 days pre-and post-partum. They used for IL-6, progesterone (P 4 ) and estradiol-17β (E 2 ) concentration determination. This study showed that the IL-6 concentration prepartum was higher than postpartum. Low levels of IL-6 and P 4 in peripheral blood prepartum tended to affect retained placenta and a high level of IL-6 prepartum tended to affect endometrit is. These results indicate that measurement of change in the IL-6 concentration during pregnancy is one useful tool for predicting crisis in postpartum reproductive diseases in dairy cattle. KEY WORDS: cattle, endometritis, interleukin-6, pregnant, retained placenta.

Abstract. This study was carried out to investigate changes in pituitary response to GnRH on gonadotrophin secretion in prepubertal heifers. A total of 50 prepubertal Holstein-Friesian heifers were treated with 1 µg/kg GnRH intravenously at 1, 2, 4, 6 and 8 months of age, and plasma samples were collected from the jugular vein at 0 to 360 min after GnRH treatment. Plasma concentrations of LH and FSH were measured by RIA. Increase in concentrations of LH and FSH, induced by GnRH, were observed in all heifers from 1 month of age, and the concentrations of LH and FSH at 30 min after GnRH treatment were significantly greater than those before GnRH treatment in heifers of all ages. The time from the GnRH administration to the appearance of the peak of LH and FSH rise was similar at each age and, was prolonged with age. The peak concentration and the amount of release from the pituitary of LH rise increased with age, while those of FSH had a tendency to decrease with age. These results indicate that the pituitary gland already has reactivity to GnRH in heifers by 1 month of age, that the capacity of LH release to GnRH in the pituitary gland develops with age, and that the regulatory mechanism for the secretion of LH and FSH develops differently in prepubertal heifers. This study suggests that the development of the capacity to secrete LH secretion in response to GnRH in the pituitary gland before puberty is one of the factors for deciding the time of the onset of puberty in heifers. Key words: GnRH, LH, Pituitary gland, Puberty (J. Reprod. Dev. 48: [545][546][547][548][549][550][551] 2002) t the puberty, LH surge release in response to GnRH surge release occurs in the pituitary gla nd, and then the rapid burst increase in peripheral LH concentration induces the first ovulation from fully-grown follicles in the ovary. B e fo r e t he fi r s t o v u la t i o n at p u b er t y , t h e hypothalamus-pituitary-gonad axis as main regulating system of reproduction has to govern. It is generally considered that the final component of the reproductive endocrine system to develop, that regulates the time of the onset of puberty in heifers and ew es, is th e hy po thal am us [1][2][3]. T he hypothalamic content of GnRH and the number of pituitary receptors for GnRH do not change during sexual ma tura tion in heifer s [4 ]. The fina l component for the onset of puberty is thought to be the development of a GnRH releasing pattern develop like in sexually mature cattle. The pattern o f G n R H r e l e a s e d e c i d e s s e c r e t i on o f gonadotrophin in the pituitary gland [5,6]. Peripheral circulating hormones, estradiol-17β and inhibin, directly or indirectly regulate GnRH and