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Association between portal endotoxemia and Child-Pugh classification in complex pathogens-induced hepatic cirrhosis in rats
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- Author:
- No author available
- Journal Title:
- WORLD CHINESE JOURNAL OF DIGESTOLOGY
- Issue:
- 15
- DOI:
- 10.3969/j.issn.1009-3079.2006.15.007
- Key Word:
- 肠源性内毒素;Child-Pugh分级;肝硬化;四氯化碳
Abstract： 目的:研究CCl4诱导大鼠肝硬化形成过程中门静脉内毒素与Child-Pugh分级,探讨肠道在大鼠肠源性内毒素及大鼠肝硬化代偿向失代偿转化中的作用.方法:20只Wistar大鼠采用CCl4复合因素诱发大鼠肝硬化模型,6只作为对照.于制模开始后的6及10 wk分别测定凝血酶原时间,白蛋白,胆红素,腹水情况,脑电图情况及门静脉内毒素水平,并依据Child-Pugh分级系统确定大鼠肝功能分级,比较Child分级与门静脉内毒素的关系.结果:经Spearman等级相关分析,Child-Pugh分级指标与白蛋白、凝血酶原时间显著相关(r=-0.695,P＜0.05;r=0.649,P＜0.05),而与胆红素没有显著相关性(r=0.111,P=0.732).门静脉内毒素水平随着肝硬化模型制作时间的延长而逐渐加重,正常大鼠门静脉内毒素水平与6及10 wk毒素门静脉内毒素水平比较均有统计学差异(925.1±527.7 mEU/L vs 1983.7±586.4,2600.7±343.8 mEU/L,均P＜0.01),门静脉内毒素水平与时间相关(r=0.624,P＜0.01),与Child-Pugh分级之间有显著相关(r=0.680,P＜0.01).结论:肝硬化大鼠门静脉高内毒素血症与肝功能分级有显著相关关系,说明肠源性内毒素在大鼠肝硬化代偿向失代偿转化中起着重要作用.
- [1]De-Wu Han.Intestinal endotoxemia as a pathogenetic mechanism in liver failure[J].2002,(6).
- [2]李夏青,韩德五,许瑞龄,等.内毒素诱发肝硬化大鼠发生肝性脑病的实验研究[J].1999,(2).
- [3]Hui-Ying Zhang,De-Wu Han,Xin-Guo Wang,etc.Experimental study on the role of endotoxin in the development of hepatopulmonary syndrome[J].2005,(4).
- [4]林敏西.肝病与肠源性内毒素血症防治[J].2003,(1).
- [5]赵龙凤,李红,韩德五.肠源性内毒素血症与肝病[J].2000,(10).
- [6]李琴,王宝恩,贾继东.肝功能分级的演变及特点：从Child到MELD[J].2004,(5).
- [7]韩德五.肠源性内毒素血症与肝病[M].2004.
- [8]D N, Mayanski,Y S, Schwartz,S N, Kutina,etc.Mononuclear phagocyte system responsiveness in CCl4-induced liver cirrhosis.[J].1993,74.
- [9]Taura P,Lacy A,Garcia-Valdecasas JC,etc.Bacterial translocation of enteric organisms in patients with cirrhosis.[J].2001,34(1).
- [10]Kuriyama S,Nagamoto I,Kikuchi E,etc.Endotoxin clearance and its relation to hepatic and renal disturbances in rats with liver cirrhosis.[J].2001,21(1).
- [11]Rodes J,Navasa M.Bacterial infections in cirrhosis.[J].2004,24(4).
- [12]K N, Oppong,K, Bartlett,C O, Record,etc.Synaptosomal glutamate transport in thioacetamide-induced hepatic encephalopathy in the rat.[J].1995,22.
- [13]Guarner C,Soriano G.Bacterial translocation and its consequences in patients with cirrhosis.[J].2005,17(1).
- [14]D N, Maianski,Ia Sh, Shvarts,D D, Tsyrendorzhiev,etc.[Functional restructurings of the mononuclear phagocyte system in experimental liver cirrhosis].[J].1988,105(2).
- [15]Mazmanian M,Herve P,Libert JM,etc.Cirrhotic rats with bacterial translocation have higher incidence and severity of hepatopulmonary syndrome.[J].2005,20(10).
- [16]韩德五,马学慧,赵元昌.肝硬化动物模型的研究[J].1979,(4).
- [17]韩德五.肠源性内毒素血症所致"继发性肝损伤"的临床依据[J].1999,(12).
- [18]S W, Luckey,D R, Petersen.Activation of Kupffer cells during the course of carbon tetrachloride-induced liver injury and fibrosis in rats.[J].2001,71(3).
- [19]Yano H,Kinoshita S,Kira S.Effects of acute moderate exercise on the phagocytosis of Kupffer cells in rats.[J].2004,182(2).
- [20]Such J,Aparicio JR,Pascual S,etc.Intestinal permeability is increased in patients with advanced cirrhosis.[J].2003,50(53).
- [21]John Lough,Leonard Rosenthall,Artin Arzoumanian,etc.Kupffer cell depletion associated with capillarization of liver sinusoids in carbon tetrachloride-induced rat liver cirrhosis[J].1987,5(2).
- [22]S, Arii,K, Monden,S, Itai,etc.Depressed function of Kupffer cells in rats with CCl4-induced liver cirrhosis.[J].1990,190(3).