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Liver resection for the treatment of post-cholecystectomy biliary stricture with vascular injury 被引量:3
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作者 Marcos V Perini Paulo Herman +5 位作者 Andre L Montagnini Jose Jukemura Fabricio F Coelho Jaime A Kruger telesforo bacchella Ivan Cecconello 《World Journal of Gastroenterology》 SCIE CAS 2015年第7期2102-2107,共6页
AIM:To report experience with liver resection in a select group of patients with postoperative biliary stricture associated with vascular injury.METHODS:From a prospective database of patients treated for benign bilia... AIM:To report experience with liver resection in a select group of patients with postoperative biliary stricture associated with vascular injury.METHODS:From a prospective database of patients treated for benign biliary strictures at our hospital,cases that underwent liver resections were reviewed.All cases were referred after one or more attempts to repair bile duct injuries following cholecystectomy(open or laparoscopic).Liver resection was indicated in patients with Strasberg E3/E4(hilar stricture)bile duct lesions associated with vascular damage(arterial and/or portal),ipsilateral liver atrophy/abscess,recurrent attacks of cholangitis,and failure of previous hepaticojejunostomy.RESULTS:Of 148 patients treated for benign biliary strictures,nine(6.1%)underwent liver resection;eight women and one man with a mean age of 38.6 years.Six patients had previously been submitted to open cholecystectomy and three to laparoscopic surgery.The mean number of surgical procedures before definitive treatment was 2.4.All patients had Strasberg E3/E4injuries,and vascular injury was present in all cases.Eight patients underwent right hepatectomy and one underwent left lateral sectionectomy without mortality.Mean time of follow up was 69.1 mo and after longterm follow up,eight patients are asymptomatic.CONCLUSION:Liver resection is a good therapeutic option for patients with complex postoperative biliary stricture and vascular injury presenting with liver atrophy/abscess in which previous hepaticojejunostomy has failed. 展开更多
关键词 ABSCESS ATROPHY BENIGN BILE ducts CHOLECYSTECTOMY
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Pentoxifylline enhances the protective effects of hypertonic saline solution on liver ischemia reperfusion injury through inhibition of oxidative stress 被引量:3
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作者 Vinicius Rocha-Santos Estela RR Figueira +5 位作者 Joel A Rocha-Filho Ana MM Coelho Rafael Soraes Pinheiro telesforo bacchella Marcel CC Machado Luiz AC D'Albuquerque 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS CSCD 2015年第2期194-200,共7页
BACKGROUND:Liver ischemia reperfusion(IR)injury triggers a systemic inflammatory response and is the main cause of organ dysfunction and adverse postoperative outcomes after liver surgery.Pentoxifylline(PTX)and h... BACKGROUND:Liver ischemia reperfusion(IR)injury triggers a systemic inflammatory response and is the main cause of organ dysfunction and adverse postoperative outcomes after liver surgery.Pentoxifylline(PTX)and hypertonic saline solution(HTS)have been identified to have beneficial effects against IR injury.This study aimed to investigate if the addition of PTX to HTS is superior to HTS alone for the prevention of liver IR injury.METHODS: Male Wistar rats were allocated into three groups. Control rats underwent 60 minutes of partial liver ischemia, HTS rats were treated with 0.4 mL/kg of intravenous 7.5% NaCl 15 minutes before reperfusion, and HPTX group were treated with 7.5% NaC1 plus 25 mg/kg of PTX 15 minutes before reperfusion. Samples were collected after reperfusion for determination of ALT, AST, TNF-α, IL-6, IL-10, mitochondrial respiration, lipid peroxidation, pulmonary permeability and myeloperoxidase. RESULTS: HPTX significantly decreased TNF-α 30 minutes after reperfusion. HPTX and HTS significantly decreased ALT,AST, IL-6, mitochondrial dysfunction and pulmonary myelo- peroxidase 4 hours after reperfusion. Compared with HTS only, HPTX significantly decreased hepatic oxidative stress 4 hours after reperfusion and pulmonary permeability 4 and 12 hours after reperfusion. CONCLUSION: This study showed that PTX added the beneficial effects of HTS on liver IR injury through decreases of hepatic oxidative stress and pulmonary permeability. 展开更多
关键词 PENTOXIFYLLINE hypertonic saline solution hepatic oxidative stress ischemia reperfusion injury pulmonary permeability
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Pentoxifylline 通过 TNF- 合成和 TGF-1 基因表示的下面规定改进肝新生 被引量:2
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作者 Rodrigo Bronze Martino Ana Maria Mendona Coelho +5 位作者 Márcia Saldanha Kubrusly Regina Leito Sandra Nassa Sampietre Marcel Cerqueira Cesar Machado telesforo bacchella Luiz Augusto Carneiro D’Albuquerque 《World Journal of Gastrointestinal Surgery》 SCIE CAS 2012年第6期146-151,共6页
AIM:To investigate the mechanism of pentoxifylline(PTX)improvement in liver regeneration.RESULTS:Rats were randomized into 4 groups:Control rats;Sham-sham-operation rats;Saline-70% hepatectomy plus saline solution;PTX... AIM:To investigate the mechanism of pentoxifylline(PTX)improvement in liver regeneration.RESULTS:Rats were randomized into 4 groups:Control rats;Sham-sham-operation rats;Saline-70% hepatectomy plus saline solution;PTX-70%hepatectomy plus PTX.At 2 and 6 h after hepatectomy,aspartate aminotransferase,alanine aminotransferase,tumor necrosis factor(TNF)-α and interleukin-6(IL-6)serum and hepatic tissue levels were determined.Tumor growth factor(TGF)-β1 gene expression in liver tissue was evaluated 24 h after hepatectomy by quantitative reverse transcriptase polymerase chain reaction analysis.Proliferation was analyzed by mitotic index and proliferating cell nuclear antigen(PCNA)staining 48 h after hepatectomy.RESULTS:TNF-α and IL-6 serum levels increased at 2 and 6 h after hepatectomy.At 2 h after hepatectomy serum PTX was reduced but not hepatic levels of TNF-α and IL-6.A decrease in liver TGF-β1 gene expression and an increase in mitotic index and PCNA after hepatectomy were observed in the PTX treatment group in comparison to the saline group.CONCLUSION:PTX improves liver regeneration by a mechanism related to down regulation of TNF-α production and TGF-β1 gene expression. 展开更多
关键词 Liver regeneration HEPATECTOMY PENTOXIFYLLINE TUMOR necrosis FACTOR α TUMOR growth FACTOR β1
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