Made available in DSpace on 2016-04-28T20:18:34Z (GMT). No. of bitstreams: 1 2009 - Ana Paula de Magalhaes Nunes.pdf: 2100747 bytes, checksum: 71718bf8a01eaa5a22f6b041a009a396 (MD5) Previous issue date: 2009-03-13 / Funda??o Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro / In order to investigate the hypothesis of the influence of serotonergic system on the control of dipsogenic and sodium appetite, we examined the effects of chronicallytreated rats with the brain serotonin releaser, fenfluramine, the 5-HT1A agonist, 8-OHDPAT and the selective serotonin re-uptake inhibitor, sertraline. Animals treated with 5- HT1A agonist and brain serotonin releaser were sodium depleted and then their fluids intake analyzed. The first group decreased significantly the salt intake response while the second group intensified the sodium appetite 2 weeks after the first administration of fenfluramine. The water consumption was not altered in none of the groups when compared to their respective controls. Sodium-depleted animals that were treated with sertraline showed a more intense natriorexigenic response. On the other hand, water deprivation induced a lower water intake in SERT-treated rats than the controls. Osmotic simulation evoked a dipsogenic response significantly lower in SERT group. Fluids and food deprivation induced a weak dipsogenic response in SERT treated-rats compared to controls but without difference on saline intake. An increased urinary density and decreased plasma sodium levels in SERT-treated rats correlated with the highest plasma vasopressin and oxytocin levels at the 3rd week post-treatment. The obtained results in chronically-treated rats with the 5-HT1A agonist and the brain serotonin releaser, suggest that the alteration on the brain serotoninergic activity influences the sodium appetite expression, possibly after 5-HT1A autoreceptor desensitization produced by 8-OH-DPAT or brain serotonin depletion achieved with fenfluramine treatment. The results of chronically-treated rats with sertraline, constitute the first evidence of alterations on the threshold for thirst and sodium appetite response in SERT-chronically-treated rats. These alterations possibly are consequence of the hyponatremia provided by inappropriate secretion of AVP and OT. / Para investigar a hip?tese da influ?ncia do status do sistema seroton?rgico no controle da resposta dipsog?nica e do apetite ao s?dio, analisamos os efeitos de ratos tratados cronicamente com um liberador cerebral de serotonina, fenfluramina, um agonista 5-HT1A, 8-OH-DPAT e um inibidor da recapta??o pr?-sin?ptica de serotonina, sertralina (SERT). Animais tratados com agonista 5-HT1A e com liberador cerebral de serotonina, foram submetidos a deple??o de s?dio e, posteriormente, a ingest?o de fluidos foi aferida. O primeiro grupo diminuiu significativamente a ingest?o de salina hipert?nica, enquanto o segundo grupo intensificou o apetite ao s?dio 2 semanas ap?s o ?n?cio do tratamento com fenfluramina. O consumo de ?gua n?o foi alterado em nenhum dos grupos, quando comparados aos seus respectivos grupo controle. Os animais tratados cronicamente com SERT que sofreram deple??o de s?dio, obtiveram uma intensa resposta natriorexig?nica. Por outro lado, a priva??o de ?gua induziu uma menor ingest?o de ?gua em ratos tratados cronicamente com SERT quando comparado-os aos do grupo controle. O est?mulo osm?tico evocou uma resposta dipsog?nica significativamente menor no grupo SERT. A priva??o de fluidos e de alimentos induziu uma baixa resposta dipsog?nica em ratos tratados com SERT quando comparados aos controles, mas sem diferen?a significativa na ingest?o de salina hipert?nica. O aumento da densidade urin?ria em ratos tratados com SERT correlaciona-se com os maiores n?veis plasm?ticos do horm?nio anti-diur?tico e ocitocina na 4? semana p?s-tratamento. Os resultados obtidos em ratos tratados cronicamente, com o agonista 5-HT1A e com o liberador cerebral de serotonina, sugerem uma poss?vel altera??o da atividade cerebral serotonin?rgica, influenciando assim a express?o do apetite ao s?dio, pois possivelmente ocorreu uma dessensibiliza??o de autoreceptores 5-HT1A com o tratamento com 8-OH-DPAT, e deple??o cerebral de serotonina, obtida com o tratamento com fenfluramina. Os resultados relativos aos animais tratados cronicamente com sertralina, constituem as primeiras evid?ncias de altera??o no limiar de sede e de apetite ao s?dio. Essas altera??es s?o possivelmente conseq??ncia da hiponatremia gerada pela secre??o inapropriada de ADH e OT.

Submitted by Jorge Silva (jorgelmsilva@ufrrj.br) on 2018-10-16T18:19:32Z No. of bitstreams: 1 2013 - Gabriela Ferreira de Oliveira.pdf: 1149006 bytes, checksum: e5df0fd5e246ea685fd7bb50c7ab42d5 (MD5) / Made available in DSpace on 2018-10-16T18:19:32Z (GMT). No. of bitstreams: 1 2013 - Gabriela Ferreira de Oliveira.pdf: 1149006 bytes, checksum: e5df0fd5e246ea685fd7bb50c7ab42d5 (MD5) Previous issue date: 2013-08-12 / Sodium is the major electrolyte of the extra cellular space, essential for the control of plasma osmolality and blood pressure. In addition, sodium is the only mineral for which there is a defined appetite. For sodium homeostasis and for the regulation of extra cellular fluid, the reported physiological systems include the renin angiotensin aldosterone system, atrial natriuretic peptide and oxytocin. In mice the feeding behavior of sodium is well established and the central inhibition of sodium appetite has been demonstrated. However, in some domestic species, especially in horses, subject of this study, this behavior has not yet been clarified. This study aimed to evaluate the clinical and hematological effects, beyond the assessment of fluid and electrolyte balance and feeding behavior of fluids after the central administration of enalaprilat in horses experimentally dehydrated. Six adult, gelding horses, were used. The animals were subjected to water and food restriction for 72 hours prior the study, associated with the administration of three doses of furosemide in the first 24 hours. After the 72 hours fasting, the animals were divided into two experimental groups. The first group was called Control Group (CG) and the second, Treaty Group (TG). The animals of TG received 2.75 mg/animal of enalaprilat by intracarotideal route. After administration of enalaprilat, the animals had free access to water and hypertonic saline solution (1.8% of NaCl), with ingested volumes monitored. All animals were submitted to a regular and periodical physical examination, measured blood pressure and collected blood samples every 12 hours until the administration of enalaprilat, to evaluate the effects of dehydration; and 30, 60, 120, 180 minutes and 24 hours after administration, to evaluate the drug effects. Weight loss was the parameter that best reflected dehydration, which was estimated at 10.5% at the end of 72 hours of food and water restriction. When the animals had free access to water and saline, we observed a higher total water consumption in TG (13.7 ? 12 L) than in the CG (9.1 ? 7.9 L), with no significant difference between groups (p = 0.3522). There was no significant difference between GC and GT in clinical and hematological parameters, in all moments evaluated. Evaluating the sodium appetite, as evidenced by the ratio between salt intake and the amount of fluid consumed, it was observed that the TG showed lower sodium appetite than the CG (p = 0 0396), observed 120 minutes after the central administration of enalaprilat, demonstrating the centrally action of ACE inhibitor (enalaprilat) in inhibition of sodium appetite in horses. / O s?dio ? o principal eletr?lito do espa?o extracelular, fundamental para o controle da osmolaridade plasm?tica e press?o arterial, al?m de ser o ?nico mineral para qual existe um apetite claramente definido. Para a homeostase do s?dio e do fluido extracelular, os sistemas fisiol?gicos relatados incluem o sistema renina angiotensina aldosterona (SRAA), pept?deo natriur?tico atrial (ANP) e ocitocina (OT). O comportamento ingestivo de s?dio em ratos j? est? bem estabelecido e a inibi??o central do apetite por s?dio j? foi demonstrada. Por?m, em algumas esp?cies dom?sticas, especialmente nos equinos, tema deste trabalho, este comportamento ainda n?o foi esclarecido. O objetivo deste trabalho foi avaliar os efeitos cl?nicos e hematol?gicos, al?m da avalia??o do equil?brio hidroeletrol?tico e do comportamento ingestivo de l?quidos ap?s a administra??o central de enalaprilato em equinos experimentalmente desidratados. Foram utilizados seis equinos adultos, machos, castrados, que permaneceram em jejum h?drico e alimentar por 72 horas, associado ? administra??o de furosemida. Ap?s 72 horas de jejum, os animais foram divididos em dois grupos experimentais, o Grupo Controle (GC) e o Grupo Tratado (GT), que recebeu 2,75 mg/animal de enalaprilato por via intracarot?dea. Ap?s, os animais tiveram livre acesso a ?gua e a solu??o salina hipert?nica (1,8% de NaCl). Os animais foram avaliados atrav?s de exame cl?nico, a cada 12 horas durante as 72 horas de jejum e 30, 60, 120, 180 minutos e 24 horas ap?s o Enalaprilato. Foram avaliados o peso corporal, a quantidade de l?quidos ingeridos, a press?o arterial m?dia, par?metros bioqu?micos e eletrol?ticos sangu?neos. A perda de peso corporal foi o par?metro que melhor refletiu a desidrata??o, estimada em 10,5% ao final de 72 horas de jejum. Com o restabelecimento do acesso ? ?gua e solu??o salina, observou-se maior consumo total de ?gua no GT (13,7 ? 12 L) que no GC (9,1 ? 7,9 L), sem diferen?a significativa entre os grupos (p = 0,3522). N?o houve diferen?a significativa nos par?metros cl?nicos e hematol?gicos avaliados entre o GC e o GT. O apetite por s?dio foi reduzido significativamente (p = 0, 0396) no GT comparado ao GC, evidenciado 120 minutos ap?s a administra??o do enalaprilato, demonstrando a a??o central do inibidor de ECA (Enalaprilato) na inibi??o do apetite por s?dio em equinos.