Protective effect of gastrodin on bile duct ligation-induced hepatic fibrosis in rats

Gastrodin has been showed to possess many beneficial physiological functions, including protection against inflammation and oxidation and apoptosis. Studies showed inflammation and oxidation play important roles in producing liver damage and initiating hepatic fibrogenesis. However, it has not been reported whether gastrodin has a protective effect against hepatic fibrosis or not. This is first ever made attempts to test gastrodin against liver fibrosis in bile duct ligation (BDL) rats. The aim of the present study is to evaluate the effect of gastrodin on BDL-induced hepatic fibrosis in rats. BDL rats were divided into two groups, BDL alone group, and BDL-gastrodin group treated with gastrodin (5 mg/ml in drinking water). The effects of gastrodin on BDL-induced hepatic injury and fibrosis in rats were estimated by assessing serum, urine, bile and liver tissue biochemistry followed by liver histopathology (using hematoxylin & eosin and sirius red stain) and hydroxyproline content measurement. The results showed that gastrodin treatment significantly reduced collagen content, bile duct proliferation and parenchymal necrosis after BDL. The serum alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST) decreased with gastrodin treatment by 15.1 and 23.6 percent respectively in comparison to BDL group did not receive gastrodin. Gastrodin also significantly increased the level of serum high density lipoprotein (HDL) by 62.5 percent and down-regulated the elevated urine total bilirubin (TBIL) by 56.5 percent, but had no effect on total bile acid (TBA) in serum, bile and liver tissues. The immunohistochemical assay showed gastrodin remarkably reduced the expressions of CD68 and NF-κB in BDL rats. Hepatic SOD levels, depressed by BDL, were also increased by gastrodin by 8.4 percent. In addition, the increases of hepatic MDA and NO levels in BDL rats were attenuated by gastrodin by 31.3 and 38.7 percent separately. Our results indicate that gastrodin significantly attenuated the severity of BDL-induced hepatic injury and fibrosis by attenuating oxidative stress and inflammation. Taken together, these findings suggest that gastrodin might be an effective antifibrotic drug in cholestatic liver disease.     

Telmisartan attenuates hepatic fibrosis in bile duct-ligated rats

Aim:

To evaluate the antifibrotic effect of telmisartan, an angiotensin II receptor blocker, in bile duct-ligated rats.

Methods:

Adult Sprague-Dawley rats were allocated to 3 groups: sham-operated rats, model rats underwent common bile duct ligation (BDL), and BDL rats treated with telmisartan (8 mg/kg, po, for 4 weeks). The animals were sacrificed on d 29, and liver histology was examined, the Knodell and Ishak scores were assigned, and the expression of angiotensin-converting enzyme (ACE) and ACE2 was evaluated with immunohistochemical staining. The mRNAs and proteins associated with liver fibrosis were evaluated using RTQ-PCR and Western blot, respectively.

Results:

The mean fibrosis score of BDL rats treated with telmisartan was significantly lower than that of the model rats (1.66±0.87 vs 2.13±0.35, P=0.015). However, there was no significant difference in inflammation between the two groups, both of which showed moderate inflammation. Histologically, treatment with telmisartan significantly ameliorated BDL-caused the hepatic fibrosis. Treatment with telmisartan significantly upregulated the mRNA levels of ACE2 and MAS, and decreased the mRNA levels of ACE, angiotensin II type 1 receptor (AT1-R), collagen type III, and transforming growth factor β1 (TGF-β1). Moreover, treatment with telmisartan significantly increased the expression levels of ACE2 and MAS proteins, and inhibited the expression levels of ACE and AT1-R protein.

Conclusion:

Telmisartan attenuates liver fibrosis in bile duct-ligated rats via increasing ACE2 expression level.     

医源性胆管损伤与胆管狭窄治疗体会

目的分析与研究医源性胆管损伤与胆管狭窄的原因以及治疗方法。方法本研究选择80例医源性胆管损伤与胆管狭窄的患者进行研究,利用经内腔镜逆行性胰胆管造影技术在患者体内置放支架,对医源性胆管损伤与胆管狭窄情况进行治疗,手术之后的第1、4、7及11d对患者的肝功能变化情况进行检测,对患者血白细胞水平的计算采用流式细胞术,对患者住院的时间、临床上的治愈率以及手术之后第1、3、5年的复发率进行观察。另外,还要对比分析这些患者医源性胆管损伤与胆管狭窄情况的致伤原因以及治疗结果。结果术后治愈73例患者,治愈率为91.2%,术后的第1、4、7及11d,患者总胆红素、血白细胞水平、丙氨酸转氨酶等均有显著的下降趋势。比较手术后第1d和第7d患者各项指标的数值,存在的差异具有统计学意义(P<0.05);对比第7d和第11d,各项指标之间的差异不具有统计学意义(P>0.05)。结论作为胆囊切除手术当中一种常见的并发症,医源性胆管损伤与胆管狭窄在注意遵循及掌握手术原则的前提下,大多数是可以避免的。在提高其远期疗效方面利用经内腔镜逆行性胰胆管造影技术在患者体内置放支架这种治疗方法效果显著,特别是对于胆道狭窄的直径>3mm的。     

医源性胆管损伤诊治分析

目的探讨医源性胆管损伤的原因、治疗及预防。方法回顾分析23例医源性胆管损伤。结果医源性胆管损伤多发生于胆囊切除术，胆道解剖异常、局部病理因素、术中出血及麻醉欠佳、患者体型等为其客观因素；而本组人为因素非常明显，损伤与过分自信、草率，盲目追求小切口、高速度有关。不同类型的胆管损伤应采取不同方法及早处理；术中发现者，可行裂口修补或端端吻合、T管支撑引流术，强调置管时间不少于6个月。对胆漏先行胆道及腹腔引流术，3个月后再作胆道重建术，手术方法以胆管空肠Roux—en—Y吻合最为理想。术后黄疸病例行胆管空肠Roux—cn—Y吻合术，疗效佳。结论提高医生对胆管损伤的警觉性，术中解剖清楚，是预防医源性胆管损伤的关键。     

Platelet-dependent accumulation of leukocytes in sinusoids mediates hepatocellular damage in bile duct ligation-induced cholestasis

BACKGROUND: Although it is well known that extrahepatic cholestasis induces liver damage, the mechanisms are still not completely understood. The aim of the present study was to evaluate the role of platelets and P-selectin in cholestasis-induced liver injury. EXPERIMENTAL APPROACH: C57BL/6 mice underwent bile duct ligation (BDL) and pretreatment with an anti-GP1balpha antibody, which depletes platelets, an anti-P-selectin antibody or a control antibody. Hepatic platelet and leukocyte recruitment as well as microvascular perfusion were determined by intravital fluorescence microscopy. KEY RESULTS: BDL caused significant liver damage and sinusoidal perfusion failure. BDL further induced hepatic platelet accumulation with widespread intravascular platelet aggregates, increased platelet adhesion in postsinusoidal venules and massive platelet accumulation in liver sinusoids. Administration of the anti-GP1balpha antibody reduced systemic platelet count by 90%. Depletion of platelets in BDL mice not only abolished accumulation and adhesion of platelets in sinusoids and venules but also restored sinusoidal perfusion and reduced liver enzymes by more than 83%. Platelet depletion further reduced BDL-associated sinusoidal leukocyte accumulation by 48% although leukocyte-endothelium interactions in venules were not affected. Immunoneutralization of P-selectin also inhibited hepatic microvascular accumulation of platelets and leukocytes, and protected against cholestasis-provoked hepatocellular damage. CONCLUSIONS AND IMPLICATIONS: Platelets play an important role in BDL-induced liver injury by promoting leukocyte recruitment and deteriorating microvascular perfusion. Moreover, our findings demonstrate that cholestasis-induced accumulation of platelets is mediated by P-selectin. Thus, targeting platelet accumulation may be a useful strategy against liver damage associated with obstructive jaundice.     

Effect of tetrandrine on experimental hepatic fibrosis induced by bile duct ligation and scission in rats

Tetrandrine, an alkaloid isolated from the Chinese medicinal herb Stephania tetrandra, has been shown to elicit antifibrotic effects in various cell types. In the present study, the effect of tetrandrine on liver fibrosis was investigated by using bile duct ligation and scission in rats as a model of hepatic fibrosis. Treatment with tetrandrine in fibrotic rats reduced serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase levels to 72%, 52% and 51% that of controls at 10 mg/kg/day, respectively. Liver hydroxyproline contents in tetrandrine-treated rats with bile duct ligation and scission were also reduced to 65% of that of control rats with bile duct ligation and scission at 10 mg/kg/day. The morphological characteristics of fibrotic liver, which appeared in control bile duct ligation and scission group, were improved in tetrandrine-treated bile duct ligation and scission group. We also examined the effect of tetrandrine on cultured rat hepatic stellate cells, which plays an important role in the pathogenesis of hepatic fibrosis, activation to investigate whether it could act mainly by direct action on rat hepatic fibroblastic cells. In cultured rat hepatic stellate cells, tetrandrine reduced DNA synthesis to 57% of control hepatic stellate cells at 10 microg/ml without affecting cell viability. Smooth muscle-alpha-actin expression, the phenotypic marker of activated hepatic stellate cells, was also decreased. We conclude that tetrandrine has an antifibrotic effect on liver fibrosis in rats induced by bile duct ligation and scission, indicating that it might exert a direct effect on rat hepatic stellate cells.     

肝内胆管结石合并肝门部胆管狭窄的手术处理分析

目的探讨肝内胆管结石并肝门部胆管狭窄的手术方法。方法回顾性分析我院47例肝内胆管结石并肝门部胆管狭窄手术治疗的临床资料,遵循“清除结石,解除狭窄,切除病肝,通畅引流”的原则,我们采取病肝切除、术中胆道镜检查、取石,肝门部胆管狭窄整形,胆肠R oux-en-Y大盆口吻合,空肠盲袢皮下埋置等综合治疗。术后常规消炎利胆片或中医中药预防结石复发。结果治愈45例(95.7%)。术前黄疸深重,术中渗血不止,停止手术,死亡1例,术后46天胃瘫并衰竭死亡1例。术后发现残留结石4例(8.7%),结石复发3例(6.5%),优良率93.7%;术后并发胆汁漏3例(6.5%),残留结石术后6周经T管窦道取净结石4例。结石复发的3例中经切开皮下空肠盲袢纤维胆道镜取石成功1例,再手术切除狭窄胆肠吻合口,重新行胆管空肠吻合,并应用纤维胆道镜取石2例。结论术前完善的检查对于了解肝内胆管结石的分布及肝门部胆管狭窄的范围有着重要的意义并能为手术方案的制订提供积极的指导作用。病变肝叶或肝段切除、肝门部狭窄胆管大范围切开整形、术中应用纤维胆道镜检查、取石、并建立皮下便捷通道的肝胆管空肠R oux-en-Y大盆口吻合是治疗该疾病的首选综合治疗方法。术后常规用药预防结石复发也是必要的。     

Bifendate treatment attenuates hepatic steatosis in cholesterol/bile salt- and high-fat diet-induced hypercholesterolemia in mice

Effects of bifendate, a synthetic intermediate of schisandrin C (a dibenzocyclooctadiene derivative), on liver lipid contents were investigated in experimentally-induced hypercholesterolemia in mice. Hypercholesterolemia was induced by either chronic administration of cholesterol/bile salt or feeding a high-fat diet containing cholesterol and/or bile salt. Hepatic and serum total cholesterol levels were significantly increased (42-268% and 23-124%, respectively) in cholesterol or high-fat diet-treated mice, when compared with control animals receiving vehicle or normal diet. Hepatic triglyceride level was increased (up to 108%), but serum triglyceride level was significantly reduced by 23-63% in hypercholesterolemic mice. Daily administration of bifendate (0.03-1.0 g/kg, i.g.) for 4 days decreased hepatic levels of total cholesterol (9-37%) and triglyceride (10-37%) in hypercholesterolemic mice. Supplementing the high-fat diet with bifendate (0.25%, w/w) caused decreases in hepatic total cholesterol (25-56%) and triglyceride (22-44%) levels following 7 or 14 days of experiment, respectively, when compared with animals fed with high-fat diet not supplemented with bifendate. While fenofibrate treatment decreased both hepatic and serum lipid levels in hypercholesterolemic mice, bifendate treatment did not reduce serum lipid levels. Bifendate and fenofibrate caused an increase (10-41% and 59-98%, respectively) in hepatic index of hypercholesterolemic mice. The results indicate that bifendate treatment can invariably decrease hepatic (but not serum) lipid levels in various mouse models of hypercholesterolemia.     

胆管损伤的分型和预防

腹腔镜胆囊切除术是普外科开展最广泛的手术之一。胆管损伤是小慨率事件,一旦发生后果严重,正确的损伤分型关乎到损伤修复的效果和患者的长期生活质量。预防腔镜胆囊切除术中胆管损伤越来越受到关注,探讨胆管损伤的分型和损伤的预防措施有非常重要的临床意义。     

Platycodin D protects against cigarette smoke-induced lung inflammation in mice

Cigarette smoke is the one of the major factors that leads to chronic obstructive pulmonary disease (COPD). Inflammation and oxidant stress have been known to play critical roles in the development of COPD. Platycodin D (PLD) has been reported to have anti-inflammatory and anti-oxidant effects. In this study, we aimed to investigate the protective effects of PLD on cigarette smoke (CS)-induced lung inflammation in mice. PLD was adminstrated i.p. to mice 2 h before CS exposure daily for five consecutive days. The production of inflammatory cytokines TNF-α and IL-1β were measured by ELISA. The levels of malonaldehyde (MDA) and nitric oxide (NO) were also detected in this study. The expression of nuclear factor-erythroid 2–related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NF-κB, and IκBα were detected by western blot analysis. The results showed that PLD significantly attenuated CS-induced lung pathological changes, inflammatory cells infiltration, as well as TNF-α and IL-1β production. CS-induced MDA and NO production were also inhibited by treatment of PLD. Western blot analysis showed that PLD significantly suppressed CS-induced NF-κB activation. In addition, PLD was found to increase the expression of Nrf2 and HO-1. Taken together, these results indicated that PLD protected against CS-induced lung inflammation by inhibiting inflammatory and oxidative response through activating Nrf2 signaling pathway. PLD might be an effective treatment for CS-induced lung inflammation.     

Chloroquine attenuates paraquat-induced lung injury in mice by altering inflammation,oxidative stress and fibrosis

Paraquat is one of the most extensively used herbicides and has high toxicity for humans and animals. However, there is no effective treatment for paraquat poisoning. The aim of the present study was to evaluate the effects of chloroquine on paraquat-induced lung injury in mice. Mice received a single intraperitoneal injection of paraquat and a daily intraperitoneal injection of the indicated dosages of chloroquine or dexamethasone. The histological changes, inflammation and oxidative stress in the lungs were examined at day 3, and the degree of pulmonary fibrosis was examined at day 28. H&E staining showed that chloroquine markedly attenuated lung injury induced by paraquat. In addition, the inflammatory responses induced by paraquat were inhibited after treatment with chloroquine, as indicated by the decreased number of leukocytes, the reduced levels of TNF-α, IL-1β and IL-6 in the bronchoalveolar lavage fluid, the reduced NO content, and downregulation of iNOS expression in lung tissues. No different effect was found between high-dose chloroquine and dexamethasone. Additionally, the treatment with chloroquine increased the activity of SOD and decreased the level of MDA in the lung tissues. The expressions of the anti-oxidative proteins, Nrf2, HO-1 and NQO1, were also upregulated by chloroquine treatment. The high-dose chloroquine was more effective than dexamethasone in its anti-oxidation ability. Finally, the results of Masson's staining illustrated that chloroquine markedly attenuated fibrosis in the paraquat-exposed lungs. Immunohistochemistry staining showed that the expressions of the pro-fibrotic proteins TGF-β and α-SMA were downregulated after treatment with chloroquine. In conclusion, chloroquine effectively attenuated paraquat-induced lung injury in mice.     

Diet stimulation as a synergistic factor of aggravation in a pancreatic bile duct ligation-induced rat pancreatitis model

We evaluated the association between aggravation of pancreatitis and multiple factors enhancing pancreatic exocrine secretion using a rat model of pancreatic bile duct ligation (PBDL)-induced pancreatitis. Under fasting and non-fasting conditions, a PBDL group, a second group treated by hepatic bile duct ligation (BDL) and a third group treated by pancreatic duct ligation (PDL) were compared in terms of serum amylase (S-amylase) activity. The S-amylase activity in the PBDL group was higher than in the sham group. In the PDL group, the increase in S-amylase activity was lower than in the PBDL group. In the BDL group, no increase in S-amylase activity was observed. Diversion of pancreatic and/or bile juice in these groups resulted in no increase of S-amylase activity. Truncal vagotomy or injection of an anticholinergic drug or a cholecystokinin (CCK)1-receptor antagonist inhibited pancreatic exocrine secretion and S-amylase activity in the non-fasting PBDL group but not in the fasting PBDL group. These results suggest that retention of pancreatic juice in the pancreatic duct is necessary for the increase of S-amylase activity, and that dietary stimulation and impaired duodenal inflow of bile and pancreatic juice commonly enhance pancreatic exocrine secretion, acting synergistically as aggravating factors in pancreatitis. CCK and the vagus nerve system appears to be involved in enhancing pancreatic exocrine secretion with diet stimulation as an aggravating factor.     

Docosahexaenoic acid attenuates carbon tetrachloride-induced hepatic fibrosis in rats

Fish oil containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) has been reported to exert beneficial health effects, including hepatoprotection. However, the effect of DHA alone has not been well studied, and the mechanism is not fully understood. In the present study, we reported the protective effect of DHA on carbon tetrachloride (CCl₄) induced hepatic fibrosis. Compared with the control group, the CCl₄ group showed hepatic damage as evidenced by histological changes and elevation in serum transaminase activity, fibrosis, inflammation and oxidative stress levels. These pathophysiological changes were attenuated by chronic DHA supplementation. The anti-fibrotic effect of DHA was accompanied by reductions in gene and protein expression of α-smooth muscle actin (α-SMA), fibronectin, and collagen in the liver tissue. DHA also attenuated CCl₄-induced elevation of lipid peroxidation (LPO) and decrease of glutathione (GSH)/oxidized GSH (GSSG) ratio. The upregulated inflammatory cytokines tumor necrosis factor (TNF)-α, interferon (IFN)-γ and interleukin (IL)-6 by CCl₄ were also ameliorated by DHA. Peroxisome proliferator-activated receptor (PPAR)-γ upregulation and type I and II receptors for transforming growth factor (TGF)-β (Tβ-RI and Tβ-RII) and platelet-derived growth factor (PDGF)-β receptor (PDGF-βR) downregulation on both mRNA and protein levels were observed by DHA treatment compared to CCl₄ group. Moreover, in vitro study showed that DHA inhibited HSC activation, being associated with elevating PPARγ level and reducing the phosphorylation levels of Smad2/3 and ERKs, which are downstream intermediates of TGFβ and PDGF receptors, respectively. Taken together, the hepatoprotective, anti-inflammatory and anti-fibrotic effects of DHA appeared to be multifactorial. Further, one of the mechanisms of the anti-fibrotic effect of chronic DHA supplementation is probably through PPARγ signaling to interrupt TGFβ/Smad and PDGF/ERK pathways in HSCs.     

医源性胆管损伤的原因及处理

目的:探讨医源性胆管损伤的原因及处理。方法:对32例医源性胆管损伤病例的临床资料进行回顾性分析。结果:本组32例,痊愈30例,治愈率93.75%,死亡2例,死亡率6.25%。4例因术后胆管狭窄再次手术,其中2例经3次手术治疗。结论:胆囊切除术是医源性胆管损伤的主要原因,提高认识、预防损伤是关键,胆管成形空肠Roux-en-Y吻合术是胆道重建术的最佳选择。     

Pantoprazole ameliorates liver fibrosis and suppresses hepatic stellate cell activation in bile duct ligation rats by promoting YAP degradation

Liver fibrosis is one of the most severe pathologic consequences of chronic liver diseases,and effective therapeutic strategies are urgently needed.Proton pump ...     

Cefmetazole excretion into the bile after hepatic portojejunostomy in congenital bile duct atresia

Antibiotics excretion into the bile was studied using CMZ which was administered by drip infusion in 12 postoperative cases of congenital bile duct atresia patients who had hepatic portojejunostomy with SURUGA II type enterostomy with the following results. Group I (correctable type children, with good bile flow, no jaundice): Excellent excretion was almost the same as that seen in adult patients. Group IIa (uncorrectable type children, with good bile flow, no jaundice): Excretion was poor but good depending on the amount of bile flow and liver function. Group IIb (uncorrectable type children, with poor bile flow, jaundice): Excretion was very poor. Group III (uncorrectable type infants, with good flow, no jaundice): Excretion was good depending on the amount of bile flow and liver function. Our study indicates that antibiotics excretion into the bile in children is closely related to the condition of the hepatic function and biliary passage.     

Aqueous extract of Artemisia iwayomogi Kitamura attenuates cholestatic liver fibrosis in a rat model of bile duct ligation

Cholestatic liver fibrosis, characterized by excessive accumulation of extracellular matrix (ECM) proteins, is associated with bile acid-induced oxidative stress and lipid peroxidation. We evaluated the therapeutic or protective effect of an aqueous extract of Artemisia iwayomogi Kitamura (WAI) in a rat bile duct ligation (BDL)-induced hepatic fibrogenesis model. After BDL, rats were treated once daily with 25 or 50 mg/kg of WAI for 2 weeks. The serum bilirubin, aspartate transaminase, alanine transaminase, malondialdehyde, and liver hydroxyproline levels were drastically increased in the BDL group. WAI administration significantly reduced these markers and restored BDL-induced depletion of glutathione content and glutathione peroxidase activity. Cholestatic liver injury and collagen deposition were markedly attenuated by WAI treatment, and these changes were paralleled by significantly suppressed gene and protein expression of fibrogenic factors, including hepatic alphasmooth muscle actin, platelet-derived growth factor, and transforming growth factor β. Our data suggest that WAI may have antifibrotic properties via both improvement of antioxidant activities and inhibition of ECM protein production in the rat model of BDL.     

Effect of sodium butyrate on gastric ulcer aggravation and hepatic injury inflicted by bile duct ligation in rats

Background and AimCholestasis is positively associated with an increased risk of peptic ulceration. The present study investigated the aggravating effect of cholestasis on piroxicam-induced gastric ulceration. The study also evaluated the effect of sodium butyrate (SoB) on piroxicam-induced gastric ulceration in cholestatic animals and its effect on hepatic tissues and both effects were compared to ursodeoxycholic acid (UDCA) as a standard anticholestatic drug.MethodsBile duct ligation was adopted for induction of cholestasis in rats. The cholestatic animals received saline, SoB (P.O, 400 mg/kg, twice daily) or UDCA (P.O, 30 mg/kg/day) for 4 days starting from the first day of surgery. On the 4th day, blood samples were collected for determination of serum hepatic markers, then gastric ulcers were induced by piroxicam administration (P.O, 50 mg/kg) and 4 h later, the stomach was isolated and gastric mucosa was collected for biochemical determinations. The ulcer indices for the investigated drugs were compared to omeprazole as a standard acid suppressive drug.ResultsPiroxicam-induced ulceration was exacerbated in cholestatic rats. Gastric mucosa showed a significant elevation of MDA and TNF-α together with a significant decrease in GSH &VEGF levels. SoB treatment significantly attenuated ulcer development. The afforded protection was higher than that provided by UDCA and was not significantly different from that afforded by omeprazole. SoB significantly decreased gastric mucosal MDA and TNF-α level, whereas UDCA failed to alter these parameters. Both drugs significantly elevated GSH, VEGF and IL10 levels. Similar to UDCA, SoB showed a significant reduction in AST, ALT, GGT, ALP and bilirubin level. Histopathological examination confirmed the attenuating effect of SoB on gastric and hepatic injury.ConclusionsSodium butyrate effectively protected gastric and hepatic tissues against cholestasis-induced damage. Gastroprotection was mediated through antioxidant, anti-inflammatory and angiogenic activities.     

腹腔镜胆囊切除术胆管损伤的防治体会

目的：探讨腹腔镜胆囊切除术中胆管损伤的原因及防治方法。方法：回顾性分析2004～2006年的527例腹腔镜胆囊切除术,其中胆管损伤6例,包括胆总管横断2例,胆总管夹闭1例,胆囊管残端漏1例,胆囊迷走胆管损伤2例。胆总管损伤患者均行一期手术,胆囊迷走胆管损伤患者置管引流治愈。结果：本组患者1例因发生胆管狭窄后再次手术行Roun-en-y吻合术,其它患者恢复顺利。结论：严格规范的操作,胆囊三角良好的显露,辨清肝总管、胆总管和胆囊管之间的关系,必要时中转开腹,是避免肝外胆管损伤和预防胆漏的关键。     

不同肝门胆管成形胆道重建术治疗肝门部胆管狭窄的疗效分析

目的探讨不同手术方式治疗肝门胆管狭窄的临床效果。方法将43例胆管结石合并肝门胆管炎性狭窄患者分为实验组23例与对照组20例。实验组进行带胆囊瓣血管蒂肝门胆管成形术,对照组进行胆管空肠Roux-en-Y吻合术。比较两组胆漏发生率、结石复发率及术后胆管炎发生率。结果两组术后胆漏的发生率差异无统计学意义(P>0.05),实验组结石复发率为4.3%,对照组结石复发率为25.0%,实验组结石复发率低于对照组(P<0.05);实验组术后胆管炎发生率为8.7%,对照组术后胆管炎发生率为30.0%,实验组胆管炎发生率低于对照组(P<0.05)。结论带胆囊瓣血管蒂肝门胆管成形术治肝门部胆管狭窄具有较好疗效。