The ovaries and the uterine as well as vaginal mucous membranes of 80-, 180-and 365-day-old intact female rats and females neonatally treated with a single dose of oestrogen and repeated doses of human chorionic gonadotropin (D+/ were studied. Numerous follicles, interstitial cells and corpora lutea (CL) were Key words: Rat, ovary, uterus, vagina, oestrogen, hCG The progressive decline of regular oestrous cycles and ovulatory functions with advancing age in female rats has been well documented in previous studies (Pantic and Lovren, 1981;Ennis and Davies, 1982;Nass et al., 1984). In female rats and mice, neonatal oestrogen treatment induces changes in the reproductive tract that may persist throughout the animals life (Pantic, 1981). These changes include a persistent rather than cyclic oestrus. During persistent oestrus, circulating oestradiol is present from many large ovarian follicles, but the luteinizing hormone surge mechanism is inhibited and ovulation does not occur (Leung, 1978;Pantic and Lovren, 1981).Studies on abnormalities of the reproductive tract indicate that oestrogens have inhibitory effects on ovarian steroidogenesis (Groen-Clevant, 1981;Wada et al., 1984). The uterus and vagina are also dependent on the effect of hormones administered to neonates (Ennis and Davies, 1982;Keys and King, 1989).In this paper, attention is focused on the ovarian follicles and interstitial tissue and on the properties of uterus and vagina in adult rats neonatally treated with oestrogen and human chorionic gonadotropin (hCG).
The consequences of peri-parturient Monensin administration were studied in two dairy herds in ≥ 2 parity HF cows (1) calving in moderate body condition (score, BCS: 3.25-3.75) and producing ≥8500 kg FCM in the previous lactation (Herd K), as well as (2) in those being overfed before calving (BCS: ≥3.75), but producing less milk (5-8000 kg FCM) (Herd S). In both herds on days 249-256 of gestation half of the cows received an intraruminal constant release capsule of Monensin (Rumensin® capsule, ELANCO) (Monensin-K and Monensin-S cows), the others remained untreated controls (Control-K and Control-S cows). Blood samples were taken on day 1-3 after calving and again 4 times with 7 days intervals to assay certain hormones and metabolites. On days 1-3 and again on days 28-35 also the ACTH induced Cortisol response and TRH induced T4/T3 responses were determined. The resumption of ovarian cyclicity was followed by milk progesterone profiles. In the first 10 weeks after calving the milk production of Monensin-K cows (n=13) did not differ from that of Control-K cows (n=14). The cows lost their body weight continuously in the first 10 weeks of lactation in Herd S, whereas only in the first 5 weeks in Herd K. Monensin only slightly influenced the degree of weight loss (on both farms), and the circulating leptin level (determined only in Herd S). Significantly lower insulin, IGF-1, T4, T3, glucose and cholesterol levels as well as less elevated βOH-butyrate and non-esterified fatty acid concentrations were seen in Control-S (n=13) than in Monensin-S (n=ll) cows, first of all in the first two weeks after calving. These ionophor-related differences were less obvious or disappeared in Herd-K. Monensin shortened the postpartum acyclic and anestrous periods as well as the calving to re-conception interval but this effect was significant only in the Herd S.
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