PURPOSE: To investigate superoxide dismutase (SOD) activity in the portal vein endothelium and malondialdehyde acid (MDA) production in liver tissue of rats submitted to 70% hepatectomy. METHODS:Twelve rats were distributed in two groups (hepatectomy and sham). Animals were sacrificed on post operative day 1 and portal vein, liver tissue and blood samples were collected. Portal vein SOD production was measured using lucigenin-amplified chemiluminescence assays. MDA measurement was used as an index of oxidative stress through the formation of TBARS (Thiobarbituric Acid Reactive Species). RESULTS: There was no difference in post operative bilirrubin, AST, ALT levels between groups. DHL level was higher in the hepatectomy group (p=0.01). MDA production in the remnant liver tissue and endothelial portal vein SOD activity were also significantly (p<0.05) elevated in the hepatectomy group when compared to control group. There was no correlation between MDA and SOD activity. SOD activity, on the other hand, showed a positive correlation with LDH level (p=0.038) and MDA levels showed a positive correlation with AST and ALT levels (p<0.001). CONCLUSION: There is an increased production of malondialdehyde acid in liver tissue after partial hepatectomy and increased activity of superoxide dismutase in portal vein endothelium as well.

OBJETIVO: Investigar o efeito do bloqueador opióide naltrexone na resposta inflamatória da pancreatite aguda. METODOS: Pancreatite aguda foi induzida em ratos machos Wistar, através de injeção retrógada de solução de taurocolato de sódio a 2,5% nos ductos pancreáticos. Os animais foram alocados em dois grupos: Grupo controle (n=9) animais receberam 0,5 ml de solução salina intra-peritonial 15 minutos antes da indução da pancreatite aguda e Grupo naltrexone (n=9) animais receberam naltrexone (15mg/kg de peso), em 0,5 ml de volume final por via intraperitoneal, 15 minutos antes da indução da pancreatite aguda. Foram avaliados o volume de ascite, os níveis séricos de amilase e IL-6, assim como TNF-α peritoneal e a atividade da mieloperoxidase (MPO) no tecido pulmonar. RESULTADOS: Não foram encontradas diferenças significantes nos parâmetros analisados entre o grupo que recebeu solução salina e o que recebeu naltrexone . CONCLUSÕES: Os receptores opióides não desempenham papel importante na resposta inflamatória sistêmica associada à pancreatite aguda. Se os opioides alteram a sinalização inflamatória nos leucócitos está ação não se reflete na patogênese da pancreatite aguda

PURPOSE: To investigate the effect of the opioid blocker naltrexone in the inflammatory response in acute pancreatitis (AP). METHODS: Acute pancreatitis was induced in anesthetized male Wistar rats by retrograde injection of 2.5% sodium taurocholate diluted in 0.5ml saline into the main pancreatic duct. Animals were randomized to the following experimental groups: Control Group (n=9): animals received an intraperitoneal injection of saline solution (0.5ml), 15 minutes before the induction of AP. Naltrexone Group (n=9): animals received an intraperitoneal injection of naltrexone 0.5ml (15 mg/kg), 15 minutes before induction of AP. Peritoneal levels of TNF-α and serum levels of IL-6 and amylase were determined The volume of the ascitic fluid was also evaluated. Myeloperoxidase (MPO) activities were analyzed in homogenates of pulmonary tissue. RESULTS: There were no significant differences in the ascitic fluid volume, nor in TNF-a and IL-6 levels in the naltrexone group compared to controls. Treatment with naltrexone did not affect the lung MPO activity compared to control group. CONCLUSIONS: The opioid receptors don't play an important role in the pathogenesis of the inflammatory response in acute pancreatitis. If opioids affect leukocytes inflammatory signaling, there are no major implications in the pathogenesis of acute pancreatitis.

OBJETIVO: Desenvolver um modelo cirúrgico de IHA e hiperamonemia em ratos, que evita o shunt porto-sistêmico e a ligadura do ducto biliar, que seja aplicável à pesquisa de encefalopatia hepática. MÉTODOS: Após anestesia geral e laparotomia mediana, os pedículos dos lobos laterais direito e caudado foram isolados e clampeados. Após 1 hora, o animal foi reaberto, os clampes retirados e foi realizada hepatectomia anterior subtotal (ressecção dos lobos médio e lateral esquerdo), compreendendo a remoção de 75% do parênquima. Quatro horas após a hepatectomia, amostras de sangue e tecido hepático foram coletadas nos grupos IHA e controle. RESULTADOS: Diferenças entre os grupos IHA e controle foram significativas para ALT, AST, bilirrubina total e direta, sódio, potássio, fosfatase alcalina, gama glutamiltransferase e principalmente amônia. Histologicamente, diferenças significativas foram observadas entre os grupos. CONCLUSÃO: O modelo é útil para o estudo de aspectos específicos da IHA e o desenvolvimento de novas abordagens terapêuticas.

PURPOSE: To develop a reliable surgical model of acute hepatic failure and hyperammonemia in rats that avoids porto-systemic shunt and bile duct ligation, applicable to hepatic encephalopathy research. METHODS: The pedicles of right lateral and caudate lobes were exposed and clamped. One hour later, the animal was reopened, clamps were released and anterior subtotal hepatectomy (resection of median and left lateral lobes) was performed, comprising 75% of liver removal. Four hours after hepatectomy, blood samples and liver tissues were collected from ALF and control groups. RESULTS: Differences between ALF and control groups were significant for ALT, AST, total and direct bilirubin, sodium, potassium, alkaline phosphatasis, gamma-glutamyltransferase and most important, ammonia. Histologically, significant differences were noticed between groups. CONCLUSION: The model is useful for the study of specific aspects of ALF and the development of new therapeutic approaches.

OBJETIVO: Determinar se a dieta enriquecida com rosiglitazona oferece proteção em um modelo clássico de lesão de isquemia e reperfusão hepática em ratos. MÉTODOS: Dois dias antes do experimento, os ratos foram divididos em 2 grupos: Grupo Controle (n=13): ratos alimentados com dieta padrão; Grupo Rosi (n=13): ratos alimentados com dieta em pó padrão enriquecida com rosiglitazona. Os animais foram submetidos à isquemia e reperfusão hepática por clampeamento do pedículo dos lobos médio e anterolateral esquerdo. Após 1 hora de isquemia, o clampe foi removido para a reperfusão. Após 2 ou 24 horas (Grupos Controle e Rosi), o sangue foi coletado para análise de enzimas e citocinas. Os fígados isquêmico e não isquêmico foram coletados para análise de malondialdeído e avaliação histológica. Pulmões foram removidos para quantificação da mieloperoxidase tecidual. RESULTADOS: Não houve diferenças estatísticas entre grupos em todos os parâmetros analisados. CONCLUSÃO: Nesse modelo, a dieta enriquecida com rosiglitazona não protegeu contra a lesão de isquemia e reperfusão hepática.

PURPOSE: To determine whether rosiglitazone-enriched diet offer protection in a classical model of liver ischemia-reperfusion injury in rats. METHODS: Two days before the experiment, rats were divided into 2 groups: Control Group (n=13) rats fed with standard diet; Rosi Group (n=13): rats fed with a powdered standard diet supplemented with rosiglitazone. The animals were submitted to liver ischemia-reperfusion by clamping the pedicle of median and left anterolateral lobes. After 1 hour of partial hepatic ischemia, the clamp was removed for reperfusion. After 2 or 24 hours (Control and Rosi Groups), blood was collected for enzymes and cytokines analysis. Ischemic and non-ischemic liver were collected for malondialdehyde analysis and histological assessment. Lungs were removed for tissue myeloperoxidase quantification. RESULTS: There were no statistical differences between groups for all analysed parameters. CONCLUSION: In this model, rosiglitazone-enriched diet did not protect liver against ischemia-reperfusion injury.