Efeito de lipopolissacarídeo de Escherichia coli no apetite ao sódio

• Ano de defesa: 2009
• Autor(a) principal: Almeida, Roberto Lopes de
• Orientador(a): Luca Júnior, Laurival Antonio de
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Carlos
• Programa de Pós-Graduação: Programa Interinstitucional de Pós-Graduação em Ciências Fisiológicas - PIPGCF
• País: BR
• Palavras-chave em Português: Fisiologia; Equilíbrio hidroeletrolítico; Sede; Pressão arterial; Apetite ao sódio; Endotoxina; Receptores adrenérgicos; Sepse
• Palavras-chave em Inglês: Sodium appetite; Thirst; Endotoxin; Adrenoceptors; Arterial pressure; Sepsis
• Área do conhecimento CNPq: CIENCIAS BIOLOGICAS::FISIOLOGIA
• Link de acesso: https://repositorio.ufscar.br/handle/20.500.14289/1263

Lipopolysaccharide (LPS), an endotoxin derived from gram-negative bacteria wall, triggers a conjunct of systemic and behavioral responses grouped under the name of sickness behavior. Several works show the inhibition of ingestive behavior in animals with activated immune system by systemic LPS. The aim of this work was demonstrate that LPS inhibit sodium appetite in lower doses than those that cause lethal effects and that LPS inhibitory action on sodium appetite involves α2 adrenergic mechanisms. Were produced three works where we show the LPS effects on sodium appetite, on arterial pressure and in different kinds of thirst. In the first work, we showed that LPS inhibited sodium appetite and only higher doses produced thirst inhibition, besides reduced urinary volume and natriuresis, without alterations on cardiovascular parameters in FURO/CAP-treated rats. LPS abolished intracellular thirst e reduced urinary volume and natriuresis in 2M NaCl gavage-treated animals. LPS also reduced thirst in FURO-treated animals. These results suggest that LPS has a preferential effect on sodium appetite and on thirst intracellular thirst. In the second work we showed that LPS reduce sodium appetite and that this inhibition is abolished by previous treatment with yohimbine ip, an α2 adrenoceptor antagonist in sodium depleted rats. Yohimbine when combined with LPS produced hypotension in sodium depleted rats. LPS reduced gastric empty in sodium depleted rats and this effect wasn‟t abolished by previous treatment with yohimbine. The systemic effects do not explain the inhibition on sodium appetite and we can suggest that LPS exert an inhibitory effect on sodium appetite probably mediated by central α2 adrenoceptors. In the third work we confirmed that LPS inhibit sodium appetite and that central α2 adrenergic ways mediated this response because RX-821002, an α2 adrenoceptor antagonist injected icv, abolished sodium appetite inhibition induced by systemic LPS in sodium depleted rats without produced alterations in cardiovascular parameters. All results exposed with these three works suggest that LPS inhibit sodium appetite and this inhibition is mediated by central α2 adrenoceptors.