期刊文献+

感染性胆汁中内毒素的变化及意义 被引量:6

Changes and significance of bile endotoxin in patients with bile bacterial infection
原文传递
导出
摘要 目的通过检测胆管结石病人胆汁中内毒素、内皮素(ET-1)和降钙素基因相关肽(CGRP)的浓度及血浆 ALT、AST、TB 含量,探讨内毒素在胆管结石胆道感染病人肝脏损伤中的作用。方法选择胆管结石病人50例,按临床感染程度分成择期手术组和急症手术组。另选择单纯性胆囊结石病人20例为对照组。术中采取胆总管胆汁,检测胆汁内毒素、ET-1、CGRP 和血浆 ALT、AST、TB 的含量。结果急症手术组胆汁中内毒素、ET-1、CGRP 含量和血浆 ALT、AST、TB 的含量明显高于择期手术组和对照组。伴随胆道感染程度加重,胆汁中内毒素含量升高,胆汁中 ET-1、CGRP 含量也升高,肝功能损害加重。结论胆道感染时,胆管结石病人胆汁中内毒素对肝胆系统合成和释放 ET-1、CGRP 有强烈的刺激作用。胆汁中 ET-1和 CGRP 的生理平衡失调,在胆管结石胆道感染病人肝脏损伤中可能起重要作用。 Objective To investigate the changes of endotoxin in the bile to determine the severity of liver injury in patients with bile bacterial infection. Methods A total of 50 patients with bile duct stone were divided into the selective operation group (n=26) and emergency operation group (n =24) according to the clinical symptoms and signs. Twenty patients with simple gallbladder stone were selected to serve as the control group. The levels of endotoxin, endothelin-1 (ET-1) and calcito- nin gene-related peptide (CGRP) in the bile were determined during the operation and those of ALT, AST and TBil in the blood were measured before the operation. Results The levels of endotoxin, ET-1 and CGRP in the bile and plasma levels of ALT, AST and TBil were significantly higher in the emergency operation group than in the selective operation group and control group. The levels of ET-1 and CGRP in the bile were increased and hepatic injury aggravated along with elevation of endotoxin level in the infected bile. Conclusions Endotoxin strongly stimulates the hepatobiliary system to synthesize and release ET-1 and CGRP. Imbalance of ET-1 and CGRP possibly plays important role in hepatic injury when bile is infected in the patients with bile duct stone.
出处 《中华肝胆外科杂志》 CAS CSCD 2006年第1期8-10,共3页 Chinese Journal of Hepatobiliary Surgery
基金 重庆市卫生局科研基金资助(渝卫01-1-018)
关键词 内毒素 胆汁 肝脏损害 Endotoxin Bile Hepatic injury
  • 相关文献

参考文献9

  • 1Parlapiano C,Paoletti V,Campana E,et al.CGRP and ET plasma levels in normal subjects.Eur Rev Med Pharmacol Sci,1999,3:139-141.
  • 2马进,李智涛.重症急性梗阻性化脓性肝胆管炎的临床特点[J].中华肝胆外科杂志,2004,10(2):89-90. 被引量:15
  • 3Choda Y,Morimoto Y,Miyaso H,et al.Failure of the gut barrier system enhances liver injury in rats:protection of hepatocytes by gut-derived hepatocyte growth factor.Eur J Gastroenterol Hepatol,2004,16:1017-1025.
  • 4龚建平,徐明清,王小丽,陈莉,李琨,韩本立.内毒素血症时肝组织中脂多糖受体CD14的表达及其意义[J].中华肝胆外科杂志,2002,8(3):175-178. 被引量:12
  • 5Lazar G Jr,Paszt A,Kaszaki J,et al.Kupffer cell phagocytosis blockade decreases morbidity in endotoxemic rats with obstructive jaundice.InflammRes,2002,51:511-518.
  • 6Ito Y,Machen NW,Urbaschek R,et al.Biliary obstruction exacerbates the hepatic microvascular inflammatory response to endotoxin.Shock,2000,14:599-604.
  • 7Chi X,Anselmi K,Watkins S,et al.Prevention of cultured rat stellate cell transformation and endothelin-B receptor upregulation by retinoic acid.Br J Pharmacol,2003,139:765-774.
  • 8Akiyoshi H,Gonda T,Terada T.A comparative histochemical and immunohistochemical study of aminergic,cholinergic and peptidergic innervation in rat,hamster,guinea pig,dog and human livers.Liver,1998,18:352-359.
  • 9Monneret G,Arpin M,Venet F,et al.Calcitonin gene related peptide and N-procalcitonin modulate CD11b upregulation in lipopolysaccharide activated monocytes and neutrophils.Intensive Care Med,2003,29:923-928.

二级参考文献15

  • 1Lai ECS, Mok FPT, Tan ESY, et al. Emergency surgery for severe acute cholangitis. Ann Surg,1990, 211:55-57.
  • 2石景森 扬毅军 见:黄洁夫 主编.急性重症胆管炎[A].见:黄洁夫,主编.腹部外科学[C].北京:人民卫生出版社,2001.1380-1388.
  • 3ULEVITCH RJ;Tobias PS.Receptor-dependent mechanisms of cell stimulation by bacterial endotoxin[J],1995(0).
  • 4Kelly JL;O'Sullivan C;O'Riordain M.Is circulating endotoxin the trigger for the systemic inflammatory response syndrome seen after injury?[J],1997.
  • 5Nieuwenhuijzen GA.Infection,the gut and the development of the multiple organ dysfunction syndrome,1996.
  • 6Davies MG;Hagen PO.Systemic inflammatory response syndrome[J],1997.
  • 7Ayala A;O'Neill P;Uebele SA.Mechanism of splenic immunosuppression during sepsis:key role of Kupffer cell mediators,1997.
  • 8Koo DJ;Chaudry IH;Wang P.Kupffer cells are responsible for producing inflammatory cytokines and hepatocellular dysfunction during early sepsis[J],1999(2).
  • 9Lichtman SN;Wang J;Lemasters JJ.LPS receptor CD14 participates in release of TNF-α in RAW 264.7 and peritoneal cells but not in Kupffer cells,1998.
  • 10Lichtman SN;Wang J;Zhang C.Endocytosis and Ca2+ are required for endotoxin-stimulated TNF-α release by rat Kupffer cells,1996.

共引文献25

同被引文献45

  • 1刘静,牛爱敏.老年急性梗阻性化脓性胆管炎PTCD治疗的临床观察与护理[J].护士进修杂志,2008,23(15):1412-1414. 被引量:6
  • 2毛笑西,杨露绮.慢性肝炎的治疗原则及目标[J].护理研究(中旬版),2005,19(7):1241-1242. 被引量:1
  • 3王剑明,肖宝来,徐立宁,邹声泉.果糖对阻塞性黄疸大鼠肝损伤及肝脏iNOS表达的影响[J].中国现代医学杂志,2006,16(8):1149-1152. 被引量:3
  • 4程南生.肝胆管结石并发症的防治[J].中国普外基础与临床杂志,2006,13(4):380-381. 被引量:10
  • 5Fogarty B J,Parks RW, Rowlands BJ,et al. Renal dysfunction in obstructive jaundice. Br J Surg. 1995. 82:877.
  • 6King LS, Kozono D, Agre P. From structure to disease: the evolving tale of aquporin Biology. Nat Rev Mol Cell Biol, 2004, 5:987-998.
  • 7Eun-Jin S, Dae-Gill K, Ho- Sub L. Protective effects of glycyrrhizin on gentamicin-induced acute renal failure in rats. Pharm Toxicol,2003. 93 : 116- 122.
  • 8Inan M,Sayek I ,Tel BC,et al. Role of endotoxin and nitric oxide in the pathogenesis of renal failure in obstructive jaundice. BrJ Surg, 1997,84:943.
  • 9Preston GM, Carroll TP, Guggino WB, el al. Appearance of water channels in xenopus oocytes expressing red cell CHIP28 protein. Science, 1992, 256:385-387.
  • 10Gong H. Wang WD, Tae-Hwan K. et al. Reduced renal ex pression of AQP2, p-AQP2 and AQP3 in haemorrhagic shockinduced acute renal failure. Nephrol Dial Transplant, 2003.18: 2551-2559.

引证文献6

二级引证文献20

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部