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| 肿瘤坏死因子在肝缺血-再灌注损伤中的作用及左旋精氨酸的干预 | |
| 引用本文： | 王万铁,林丽娜,徐正祄,谢克俭,王宗敏.肿瘤坏死因子在肝缺血-再灌注损伤中的作用及左旋精氨酸的干预[J].中国临床药理学与治疗学,2004,9(1):92-95. |
| 作者姓名： | 王万铁 林丽娜 徐正祄 谢克俭 王宗敏 |
| 作者单位： | 1. 温州医学院病理生理学教研室,温州,325027,浙江 2. 温州医学院附属一院麻醉科,温州,325027,浙江 3. 温州医学院检验系分析中心,温州,325027,浙江 4. 温州医学院附属二院病理科,温州,325027,浙江 |
| 基金项目： | 浙江省跨世纪学术和技术带头人培养基金项目(№ 992 0 86)，温州市“5 5 1人才工程”培养基金项目 (№ 98113 )，浙江省卫生厅科研基金资助项目(№ 98A0 87) |
| 摘 要： | 目的 :探讨肿瘤坏死因子 (TNF)在肝缺血 -再灌注损伤 (HIRI)中的作用及左旋精氨酸 (L Arg)对其影响。方法 :选择HIRI实验兔及肝癌手术患者 ,观察血浆TNF含量、谷丙转氨酶 (ALT)活性、肝形态学的变化及L Arg对上述指标的影响。结果 :HIRI期间 ,TNF和ALT明显升高 (P <0 .0 1) ,两者呈显著正相关 (实验兔r =0 .912 ,P <0 .0 1;患者r =0 .5 35 ,P <0 .0 1) ,肝形态学发生异常变化。使用L Arg后 ,上述指标的异常变化显著减轻 (P <0 .0 5和P <0 .0 1)。结论 :TNF是HIRI的重要发病因素 ,L Arg可通过降低TNF减轻HIRI。 |
| 关 键 词： | 缺血-再灌注损伤 肝脏 肿瘤坏死因子 左旋精氨酸 |
| 文章编号： | 1009-2501(2004)01-0092-04 |
| 修稿时间： | 2003年5月12日 |
Role of tumor necrosis factor in reperfusion injury following hepatic ischemia and effects of L-arginine |
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| WANG Wan Tie,LIN Li Na ,XU Zheng Jie,XIE Ke Jian ,WANG Zong Min.Role of tumor necrosis factor in reperfusion injury following hepatic ischemia and effects of L-arginine[J].Chinese Journal of Clinical Pharmacology and Therapeutics,2004,9(1):92-95. | |
| Authors: | WANG Wan Tie LIN Li Na XU Zheng Jie XIE Ke Jian WANG Zong Min |
| Institution: | WANG Wan Tie,LIN Li Na 1,XU Zheng Jie,XIE Ke Jian 2,WANG Zong Min 3 Department of Pathophysiology,1 Department of Anesthesiology,the First Affiliated Hospital,2 Analysis Centre,Department of Laboratary Science,3 Department of Pathology,the Second Affiliated Hospital,Wenzhou Medical College,Wenzhou 325027,Zhejiang,China |
| Abstract: | AIM: To explore the role of tumor necrosis factor (TNF) in rabbits and patients with hepatic ischemia reperfusion injury (HIRI) and the effects of L Arginine (L Arg) on the injury. METHODS: Changes of the several parameters and the effects of L Arg were observed during HIRI in 20 rabbits and 18 patients who were scheduled for elective hepatic surgery. The parameters included TNF, alanine aminotrasferase (ALT) and changes of hepatocytes morphologically. RESULTS: TNF content and ALT activities increased (P< 0.05 and P< 0.01 ), and the abnormal changes of hepatocytes morphologically were obvious during HIRI. There was positive correlation between the changes of TNF and ALT (rabbits, r= 0.912 , P< 0.01 and patients, r= 0.535 , P< 0.01 ) during HIRI. With the treatment of L Arg, the abnormal changes of all parameters as above and hepatocytes morphologically were all alleviated remarkably (P< 0.05 and P< 0.01 ). CONCLUSION: TNF may be one of the primary causes for HIRI, and L Arg can alleviate HIRI by eliminating TNF. |
| Keywords: | hepatic ischemia reperfusion injury tumor necrosis factor L arginine |
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