七氟醚预处理对LPS诱导的小鼠心功能障碍的影响  

Effects of sevoflurane preconditioning on myocardial dysfunction in lipopolysaccharide-challenged mice

作　　者：李健玲[1] 朱小青[2] 李学敏[2] 李红梅[2] 王彦平[2] 王媛[2] 戚仁斌[2] 李雅兰[1] 

机构地区：[1]暨南大学,附属第一医院麻醉科,广东广州510632 [2]暨南大学,医学院病理生理学系,国家中医药管理局病理生理实验室,广东广州510632

出　　处：《中国病理生理杂志》2012年第8期1410-1414,共5页Chinese Journal of Pathophysiology

基　　金：广东省科技计划项目(No.2009B030801032);中央高校基本科研业务费专项资金资助项目(No.21612446)

摘　　要：目的:观察七氟醚(Sevo)预处理对脂多糖(LPS)诱导的心功能障碍的影响并初步探讨其作用机制。方法:40只雄性BALB/c小鼠随机分为4组:对照组(control)、LPS组、Sevo组和Sevo+LPS组。分别用2%Sevo(以纯氧为载气)或纯氧预处理30 min,洗脱10 min后,腹腔注射LPS 18 mg/kg或等量生理盐水。于腹腔注射后12 h,通过高分辨小动物超声系统检测心功能,结束后立即采血并处死小鼠,用生化分析仪检测血清乳酸脱氢酶(LDH)和肌酸激酶同工酶(CK-MB)活性;留取小鼠心脏标本,制备石蜡切片,进行HE染色后在光学显微镜上观察各组小鼠心脏的组织结构变化,分别用硝酸还原酶法和比色法检测小鼠心肌组织中一氧化氮(NO)的含量和诱导型一氧化氮合酶(iNOS)的活性。结果:LPS腹腔注射后12 h,超声检测显示LPS组小鼠左心室舒张末期容积(LVEDV)增大(P<0.05),每搏输出量(SV)、心输出量(CO)和射血分数(EF)降低(P<0.05);血清LDH和CK-MB水平升高(P<0.05);病理切片见心肌明显病变。Sevo+LPS组与LPS组比较,LVEDV减小(P<0.05),SV、CO和EF增加(P<0.05),LDH和CK-MB水平显著降低(P<0.05),心肌组织的病理损伤减轻。LPS引起心肌组织中NO含量和iNOS活性升高(P<0.05),Sevo对此有抑制作用(P<0.05)。结论:Sevo预处理减轻LPS引起的心肌损伤和心功能障碍,其机制可能与其抑制心肌iNOS活性,减少NO的生成有关。To investigate the effects of sevoflurane （Sevo） preconditioning on myocardial dysfunction in lipopolysaccharide （LPS） - challenged mice. METHODS ： Forty male BALB/c mice were randomly allocated to 4 groups ： control group, LPS group, Sevo ＋ LPS group and Sevo group. Following pretreatment with or without 2% Sevo for 30 min and washing out for 10 rain, all mice received intraperitoneal injection of LPS or normal saline （NS）. The mice received an echocardiographic evaluation by a high - resolution in vivo imaging system 12 h after administration of ~ or NS. The mice were then killed and the hearts were removed for histological analysis. Serum levels of lactic dehydrogenase （LDH）, crea- tine kinase -MB （CK -MB） were measured with an automatic biochemical analyzer. The myocardium was homogenized for detecting the activity of inducible nitric oxide synthase （iNOS） and the content of nitric oxide （NO）. RESULTS： Ech- ocardiographic evaluation demonstrated that LPS resulted in an increase in lert ventricular end - diastolic volume and signif- icant decreases in stroke volume, cardiac output and ejection fraction. The alteration of cardiac functions was inhibited by the pretreatment with Sevo. LPS caused significant elevation of LDH and CK - MB in serum samples and severe pathologi- cal damage of the hearts. Compared with LPS group, serum levels of LDH and CK - MB were reduced and pathological damage was attenuated in Sevo ＋ LPS group. Sevo preconditioning also significantly attenuated the increases in iNOS and NO induced by LPS. CONCLUSION： Sevo preconditioning protects against myocardial impairment and myocardial dys-function in LPS - challenged mice. Inhibition of iNOS activity and of NO production by Sevo preconditioning may contribute to the beneficial role in the process of cardioprotection during endotoxemia.

关 键 词：七氟醚 预处理 脂多糖类 心肌保护 一氧化氮合酶 一氧化氮 

分 类 号：R363[医药卫生—病理学]