内源性硫化氢对实验性肝硬化门静脉高压的影响及其与一氧化氮的相互作用  

Effect of Endogenous H2 S in Experimental Hepatic Cirrhosis Portal Hypertension and Its Interaction with NO

作　　者：李文娟[1] 郑勇[2] 

机构地区：[1]蚌埠市第三人民医院急诊内科,安徽蚌埠,233000 [2]新疆石河子大学医学院第一附属医院消化内科

出　　处：《解剖与临床》2013年第5期390-393,共4页Anatomy and Clinics

基　　金：国家自然科学基金（30850004）

摘　　要：目的：探讨硫化氢（ H2 S）对实验性肝硬化门静脉高压的影响及H2 S与一氧化氮（ NO）的相互作用。方法：将32只雌性SD大鼠，随机分为肝硬化组、肝硬化＋炔丙基甘氨酸（ PPG）组、肝硬化＋硫氢化钠（ NaHS）组和正常组4组，每组8只。肝硬化组、肝硬化＋PPG组及肝硬化＋NaHS组大鼠采用四氯化碳（CCl4）复合法制备肝硬化门静脉高压动物模型。造模结束第2天，肝硬化＋PPG组大鼠腹腔注射PPG 30 mg/（kg．d），肝硬化＋NaHS组大鼠腹腔注射NaHS 56μmol/（kg．d），肝硬化组及正常组大鼠腹腔给予10 ml/（ kg．d）生理盐水。给药干预1周后，测定各组大鼠门静脉压力（ PVP）、大鼠门静脉血浆H2 S、NO含量。结果：实验结束，经病理学观察证实肝硬化大鼠模型制备成功，PVP均大于11．80 mmHg，显示门静脉高压形成。肝硬化组、肝硬化＋PPG组和肝硬化＋NaHS组PVP和门静脉血浆NO含量均高于正常组，门静脉血浆H2S含量均低于正常组（P＜0．05）。肝硬化＋PPG组PVP和门静脉血浆NO含量高于肝硬化组，门静脉血浆H2 S含量低于肝硬化组；肝硬化＋NaHS组PVP和门静脉血浆NO含量低于肝硬化组，门静脉血浆H2S含量高于肝硬化组（P＜0．05）。结论：内源性H2S对肝硬化门静脉高压发挥保护性调节作用。内源性H2 S与NO在肝硬化门静脉高压形成中可能呈现相互的负性调节作用，共同参与肝硬化门静脉高压形成的调控机制。Objective：To explore the effect of H 2 S in experimental hepatic cirrhosis portal hypertension and the interaction between hydrogen sulfide （ H2 S） and nitric oxide （ NO） .Methods：Thirty-two female SD rats were randomly divided into 4 groups（n=8） ：hepatic cirrhosis group, hepatic cirrhosis＋PPG group, he-patic cirrhosis ＋NaHS group and normal group .Rats in hepatic cirrhosis group and hepatic cirrhosis ＋PPG group and hepatic cirrhosis ＋NaHS group were subjected to CCl 4 complex methods to create a hepatic cirrhosis animal model of portal hypertension .The second day after the end of creating animal model rats in hepatic cir-rhosis＋PPG group was injected with PPG 30 mg/（kg.d）,Rats in hepatic cirrhosis＋NaHS group was injected with NaHS 56 μmol/（ kg.d） ,and rats in borh of hepatic cirrhosis group and normal groups were given 10 ml/（ kg.d） normal saline intraperitoneally .PPG an NaHS were given after 1 week, every rat portal venous pressure （ PVP） was measured with portal venous catheterization .And the plasma concentration of H 2 S and NO were measured.Results：At the end of the experiment , the hepatic cirrhosis rat model was determined by pathologi-cal.It showed the formation of portal hypertension that the portal venous pressure was higher than 11.80 mm-Hg.PPG and NaHS were given after 1 week , PVP and the plasma concentration of NO in hepatic cirrhosis group and hepatic cirrhosis ＋PPG group and hepatic cirrhosis ＋NaHS group increased in comparison with nor-mal group, and the same time, the plasma concentration of H2S were decreased,（P〈0.05）.PVP and the plasma concentration of NO in hepatic cirrhosis ＋PPG group increased in comparison with hepatic cirrhosis＆nbsp;group, and the same time , the plasma concentration of H 2 S was decreased .PVP,and the plasma concentration of NO in hepatic cirrhosis＋NaHS group decreased in comparison with hepatic cirrhosis group the same time , the plasma concentration of H2S was increased,（P〈0.05）.Conclusions：End

关 键 词：肝硬化 门静脉高压 硫化氢 一氧化氮 

分 类 号：R575.2[医药卫生—消化系统]