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机构地区:[1]山西医科大学第一医院,太原030001 [2]山西医科大学肝病研究所
出 处:《中华传染病杂志》2001年第2期94-96,共3页Chinese Journal of Infectious Diseases
基 金:卫生部科研基金!资助项目 (2 179412 )
摘 要:目的 探讨肠源性内毒素血症诱导的肝微循环障碍在肝损伤中的作用。方法 用硫代乙酰胺 (TAA)构建肠源性内毒素血症大鼠模型。 2 5只雄性Wistar大鼠分为 4组 :生理盐水组 ,肝素对照组 ,TAA组 ,TAA +肝素组。采用生化检测方法、组织化学方法和电镜技术 ,检测实验各组血浆内毒素、丙氨酸转氨酶 (ALT)和丙二醛 (MDA)水平的变化及肝组织形态学改变。结果 TAA组血浆内毒素为 (0 .1899± 0 .0 5 40 )EU/ml、ALT为 (10 0 6 .80± 91.82 )U/L、MDA为 (6 .36± 1.96 )nmol/ml;对照组分别为 (0 .0 911± 0 .0 0 6 8)EU/ml、(31.15± 10 .5 8)U/L、(3.6 6± 0 .86 )nmol/ml,两组相比TAA组明显升高 (P <0 .0 5 ) ;TAA +肝素组与TAA组相比 ,内毒素 (0 .15 97± 0 .0 35 7)略有下降 (P >0 .0 5 ) ,ALT(5 86 .6 9± 2 2 1.97)和MDA(3.6 4± 0 .95 )显著降低 (P <0 .0 5 )。肝组织形态学改变 ,苏木精 伊红染色显示TAA组肝坏死面积达 5 0 % ,纤维素染色TAA组肝窦及微血管内可见大量蓝色丝状团块样的微血栓 ;电镜结果显示TAA组窦腔内红细胞聚集、白细胞粘附贴壁 ,肝窦内皮细胞窗孔数目减少 ,而TAA +肝素组上述改变明显减轻。结论 肠源性内毒素血症可诱导肝微循环障碍导致缺血、缺氧性肝损伤 。Objective To investigate the effect of hepatic microcirculatory disturbance induced by intestinal endotoxemia in liver injury. Methods The model of rats with intestinal endotoxemia induced by thioacetamide(TAA) was established. 25 Male Wistar rats were divided into 4 groups as normal control group (N), Heparin control group(H), TAA treated group(T), and TAA+heparin treated group(T+H). The changes of plasma biochemistry and hepatic histopathology were measured. Results The plasma endotoxin level, alanine transaminase (ALT) activity and malondialdehyde (MDA) content in TAA treated rats were markedly higher than that in the control ones ( P <0.05), while plasma endotoxin level was lower ( P >0.05) and ALT as well as MDA were decreased significantly ( P <0.05) in TAA+heparin group than in TAA group. Conclusion Intestinal endotoxemia could induce disturbance of hepatic microcirculation, which results in ischemia and hypoxia of liver cell. Heparin could not only correct disturbance of hepatic microcirculation induced by intestinal endotoxemia, but also reduce liver injury induced by ischemia and hypoxia.
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