04019nam a2200205 a 450000100080000000500110000800800410001910000190006024500710007926000410015030000110019150000200020252034760022265000190369865000100371765000240372765300270375165300070377865300280378510676452018-05-25       1995    bl uuuu  m   00u1 u    #d1 aELOY, A. M. X.  aStress, opioid peptides and luteinizing hormone sevretion in ewes.  aLeeds, UK: University of Leedsc1995  a172 p.  aTese Doutorado.  aThe studies performed in this thesis aim to clarify the effects of physiologicaI and psychologicaI stresses on the plasma concentrations of cortisol and B-endorphin and the consequent effects on gonadotropin (LH) release in long-term ovariectomized ewes. AIso, a study was made of the. endogenous opioid involvement during application of these two kinds of stressors through the use of an opioid antagonist (naloxone). In this work not only was the peripheraI effect of naloxone evaluated but also its central action on the hypothalamo-pituitary adrenal axis activity and gonadotropin (LH) release. Plasma concentrations of B-endorphin and cortisol were elevated during acute (4 hours) insulin-induced hypoglycemia (2mU/kg/min) stress while plasma LH concentrations were inhibited. Infusion of the opioid antagonist naIoxone hydrochloride (5.5ug/kg/min) blocked the inhibitory effect of B-endorphin on LH release. It was concluded that endogenous opioids are involved in the control of LH release during hypoglycemia in ovariectomized ewes. In addition, this experiment detected no effect of acute hypoglycemia on episodic LH in ovariectomized animais. However, it was possible to observe a stimulatory effect of naIoxone on the LH pulse frequency in the first two hours after the beginning of the infusion, suggesting that this antagonist has short half life. During chronic (12 hours) insulin-induced hypoglycemia (2mU/kg/min), plasma ,B-endorphin levels retumed to basal levels while plasma cortisol concentrations showed a rise, suggesting incomplete feedback of corticosteroids on ACTH. LH levels remained low even during control treatment and naloxone (5.5Jlg/kg/min) infusion was not ~ble to stimulate the release of this hormone. In this case the long absence of ovarian steroids could be responsible for the lack of naloxone response and siso for the low levels of LH during saline infusion. The isolation stress that was used in this experiment allowed no visual contact but vocal communication was possible between the animaIs and lasted four hours. This caused a rise in the plasma {3-endorphin levels soon after the beginning of the stress procedure and a depression of the plasma LH leyels. Intravenous injection of naloxone (1 mg/kg) was capable of disinhibiting the LH response, suggesting the involvement of endogenous opioids in the control of LH during isolation stress. The isolation procedure did not significantly affect LH pulsatility. When the two stressors (hypoglycemia and isolation) were imposed together, plasma {3-endorphin concentrations Tose and plasma LH values were reduced. The LH pulse amplitude was affected suggesting a synergistic action of these two stressors on the GnRH pulse generator. When naIoxone (1 and 2 mg) was administered into the third ventricle to hypoglycemic animaIs made using insulin (1 mg/kg/i. v.) a blockade of the inhibitory effect of this stress on plasma LH concentrations was seen. However, naloxone had no effect on plasma LH when injected in animaIs under basal conditions. Plasma {3-endorphin and cortisol concentrations were depressed by i.c. v. injection of naloxone (2 mg) in hypoglycemic animais, but these hormones were not atfected in non-stressed animais. The intracerebroventricular injection of naloxone affected the LH pulse amplitude in hypoglycemic ewes. It is suggested that naloxone acts at the centraI nervous system, to regulate gonadotropin releasing hormone release in stressed animals.  aEndocrinologia  aOvino  aReprodução Animal  aHormônio luteinizante  aLH  aSecreção de hormônio