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Master's Dissertation
DOI
10.11606/D.5.2013.tde-20052013-162640
Document
Author
Full name
Lucas Souto Nacif
E-mail
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2013
Supervisor
Committee
Andraus, Wellington (President)
Kubrusly, Flavia Saldanha
Ribeiro Júnior, Ulysses
Title in Portuguese
Avaliação da proteína A do surfactante na síndrome hepatopulmonar em ratos
Keywords in Portuguese
Cirrose hepática experimental
Proteína A associada a surfactante pulmonar
Ratos
Síndrome hepatopulmonar
Abstract in Portuguese
INTRODUÇÃO: A síndrome hepatopulmonar (SHP) é formada por uma tríade: doença hepática, dilatação vascular intrapulmonar e alteração dos gases no sangue. Sua patogenia não está bem definida, mas especula-se que a combinação de fatores, tais como o desequilíbrio da resposta de receptores da endotelina, a remodelação microvascular pulmonar, a predisposição genética e a translocação de bactérias sejam os desencadeadores das alterações que levarão ao desenvolvimento da síndrome. O pulmão é o local principal de produção do surfactante (células alveolares epiteliais do tipo II) e desempenha um papel importante na lesão e doenças inflamatórias pulmonares. Até o momento não há relatos de avaliação do surfactante na cirrose ou na SHP. OBJETIVO: Avaliar a concentração da proteína A do surfactante na síndrome hepatopulmonar induzida em ratos. MÉTODO: Três grupos de ratos foram divididos em controle, Sham e grupo experimental de SHP. Grupo controle: somente coleta dos exames; grupo Sham: realizada a cirurgia simulada; e o grupo do modelo experimental: indução de cirrose biliar secundária através da ligadura da via biliar principal. Foi realizado a avaliação da proteína A do surfactante no homogenato pulmonar e sérico através do método imunoenzimático ELISA indireto. RESULTADOS: Observou-se depois de 28 dias a evidência de cirrose em todos os ratos operados e a apresentação de SHP em 85% dos ratos. No homogenato do pulmão no grupo LVBP e Sham, a avaliação da proteína A do surfactante (SP-A) apresentou níveis inferiores quando comparados com o grupo controle (p <0,01). No soro, a SP-A apresentou os mesmos níveis nos grupos LVBP e controle, e mostrou-se reduzida no grupo Sham. CONCLUSÃO: O modelo experimental de SHP mostrou uma redução na proteína A do surfactante no pulmão. Há também um desequilíbrio entre a proteína A do surfactante pulmonar e sérica na síndrome hepatopulmonar
Title in English
Evaluation of surfactant protein A in hepatopulmonary syndrome in rats
Keywords in English
Experimental cirrhosis
Hepatopulmonary syndrome
Protein A associated pulmonar surfactant
Rats
Abstract in English
INTRODUCTION: Hepatopulmonary syndrome (HPS) is formed by a triad: liver disease, intrapulmonary vascular dilatation and changes in blood gases. Its pathogenesis is not well defined, but it is speculated that the combination of factors such as the imbalance of endothelin receptors response, pulmonary microvascular remodeling, genetic predisposition, and bacterial translocation lead to intrapulmonary vascular dilatation. The lung is the primary site of surfactant production (alveolar epithelial type II cells) and plays an important role in inflammatory lung injury and diseases. To date, there are no reports of surfactant evaluation in cirrhosis, neither in HPS. OBJECTIVE: Evaluation of surfactant protein A in hepatopulmonary syndrome in rats. METHOD: Three groups of rats were divided into control, sham and experimental HPS groups. Control group: only exams were collected; Sham group: was performed the simulate surgery; and the experimental group: was induced secondary biliary cirrhosis. The experimental model used to induce a secondary biliary cirrhosis were the common bile duct ligation. Conducted evaluation of surfactant protein A in lung homogenate and serum by ELISA immunoassay method. RESULTS: It was observed after 28 days the evidence of cirrhosis in all operated rats. The lung homogenate surfactant protein A (SP-A) showed lower levels in HPS and sham groups in comparison with the control group (p< 0.01). In serum, the SP-A showed the same levels in HPS and control groups, and it was diminished in the sham group. CONCLUSION: The experimental model of HPS showed a reduction in surfactant protein A in lung. There is also an imbalance between lung and serum surfactant protein A levels in the hepatopulmonary syndrome
 
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Publishing Date
2013-05-21
 
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