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作 者:齐文礼[1] 宝力道[1] 吕红岩[2] 张彤[1]
机构地区:[1]内蒙古医学院第一附属医院普外科,内蒙古呼和浩特010050 [2]内蒙古自治区医院B超室
出 处:《内蒙古医学院学报》2003年第3期158-163,共6页Acta Academiae Medicinae Neimongol
基 金:内蒙古自治区自然科学基金项目 (2 0 0 1 0 90 6-1 8)
摘 要:目的 :探讨肿瘤坏死因子 (TNF-α)、一氧化氮 (NO)、内毒素 (LPS)在梗阻性黄疸 (OJ)肝细胞 (HC)超微结构损伤中的作用和相互关系及临床意义。方法 :3 2只兔随机分成四组。正常对照组 (NC组 ) 8只 ;OJ模型组2 4只 ,均做胆道结扎 (BDL)、切断复制 OJ模型 ,分别于术后 3、7、1 4d门静脉抽血测定 TNF-α、NO及血清生化指标。并对兔 HC超微结构电镜下动态观察。结果 :OJ组肝脏肿大、胆汁淤积、胆囊、胆总管近端扩张明显、充满胆汁。血清生化指标明显升高 ,以可溶性直接胆红素为主 ,证实为 OJ,与 NC组比较差异显著 (P <0 .0 1 )。血清TNF-α、NO值亦高于 NC组 ,BDL术后 7d达峰值 ,1 4d仍高于正常水平 (P <0 .0 1 )。且血清 TNF-α、NO与血清生化指标变化呈明显正相关 (r值分别为 0 .86、0 .89、 P <0 .0 1 ) ,与肝脏损伤程度和 HC超微结构损伤程度亦呈正相关。结论 :TNF-α、NO与 OJ病理过程密切相关 ,LPS诱导产生的 TNF-α、NO,是肝脏损伤 HC超微结构损伤和肝纤维化形成的重要因素。NO在此过程中似还呈现一种保护作用 。Objective: To investigate the effect and relationship between tumor necrosis factor\|alpha(TNF\|α), nitric oxide(NO) and lipopolysaccharide(LPS) on hepatocytic ultrastructure lesion in rabbits with obstructive jaundice. Methods: Thirty two rabbits were randomly divided into normal control group(NC, n=8) and bile duct ligation group(BDL, n=24). The rabbit models of obstructive jaundice were established by BDL. The levels of TNF\|α, NO and serum biochemical index were measured on 3(n=8), 7(n=8) and 14(n=8) days after operation. The rabbits hepatocytic ultrastructure were dynamically observed with transmission electron microscope. Results: Serum TNF\|α, NO levels and biochemical index in three groups were significantly high, reaching summit on 7 days after ligation and still higher than in NC group (P<0.01) after 14 days. There was a evident positive correlation between serum TNF\|α, NO, and biochemical index (P<0.01), and hepatocytic ultrastructure lesion. Conclusion: TNF\|α, NO induced by LPS can cause hepatocytic ultrastructure lesion. NO can protect liver from lesion after biliary tract obstruction and play a great part in the outcome of disease. \;
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