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This paper presents current information on the regulatory mechanism of the endocrine function of the corpus luteum in cyclic and pregnant dogs. Corpus luteum function in the first half of diestrus or pregnancy (< day 30) is independent of gonadotrophins. The mechanisms regulating corpus luteum function in this phase are largely unknown. It seems that an important role in the controlling of progesterone biosynthesis is played by StAR (steroidogenic acute regulatory protein) and 3β-HSD (3β-hydroxysteroid dehydrogenase). Recently, it has been demonstrated that prostaglandin E2 acts luteotrophically by increasing the expression of StAR. In addition, the action of progesterone on its receptors at the para-/autocrine level appears to serve as a luteotrophic factor. There is no significant difference in the regulation of corpus luteum function between pregnant and non-pregnant bitches during this time. Corpus luteum function is fully gonadotrophin-dependent during the second half of diestrus. Prolactin and, to a lesser extent, LH are the main luteotrophic factors. The slow process of luteal regression starts by day 30 after ovulation, and it takes place in spite of the increased availability of pituitary luteotrophic hormones (LH, prolactin). During luteal regression, progesterone concentration gradually decreases. This decrease is caused by a reduced expression of StAR and 3β-HSD, as well as by degenerative changes in the luteal cells. In nonpregnant bitches, progesterone concentration decreases slowly and reaches baseline values 80-90 days after ovulation. In pregnant bitches, on the other hand, progesterone decreases rapidly 1-2 days before parturition. In non-pregnant bitches, luteal regression is a passive process in the absence of luteolytic factors, whereas in pregnant bitches, luteolysis is an active process. This is due to a rapid progesterone decrease to the threshold level and the release of PGF2α from the fetal part of the placenta.
Dichlorodiphenyltrichloroethane (DDT) is a persistent insecticide, recognized as an environmental pollutant. Due to its lipophilic properties, DDT and its metabolite (DDE) are accumulated in tissues of farm animals. The aim of the study was to examine the influence of DDT and DDE on estradiol, progesterone and oxytocin secretion from the ovary and on prostaglandin (F2α and E2) secretion from the uterus, was investigated. Granulosa, luteal and endometrial cells from cows at 8-12 days of the estrous cycle were treated for 24-72 h with 0.1-10 ng/ml of DDT, p,p’-DDE, o,p’-DDE or with a technical mixture of DDE isomers. Neither DDT nor DDE were found to affect the viability of cells compared to the control. They also did not affect the secretion of estradiol from granulosa cells. The utilized pollutants increased (P < 0.05-0.001) the progesterone and oxytocin secretion from luteal and granulosa cells. They also stimulated (P < 0.05) PGF2á secretion but simultaneously reduced (P < 0.001) PGE2 secretion from endometrial cells. Hence the ratio of PGF2α to PGE2 was markedly changed, from 1:1 in the control, up to 1:4-10 in treated cells. It has been concluded that DDT and its metabolites may impair regulation of the estrous cycle in cows by stimulation of oxytocin secretion from luteal and granulosa cells and by stimulation of PGF2α and the simultaneous inhibition of PGE2 secretion from endometrial cells.
The experiment was carried out on 34 calves from birth (day 0) to 18 days of age. ACTH secretion stimulation was performed on 18 calves using arginino-vasopressine AVP Sigma, given intramuscular at a dose of 0.1 IU/kg of body weight. ACTH secretion inhibition was conducted on 16 calves by means of dexamethasone Dexaven Polfa, administered intravenously at a dose of 50 µg/kg of body weight. The hormones were administered on 0, 3, 7, 12 and 18 days after birth. Blood samples were collected between 8.00 to 8.30 a.m. The levels of ACTH and cortisol were determined in sera of the animals. The hypophysis-adrenal cortex system in calves was found to be capable of a full feedback reaction from the second week of life.
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