摘要
目的:研究蝮蛇毒蛋白C激活物(PCA)组分对败血症大鼠心脏血流动力学的影响。方法:取SD雄性大鼠24只随机分成对照组、PCA组、LPS组和LPS+PCA组四组,对照组尾静脉注射生理盐水,PCA组尾静脉注射蝮蛇毒蛋白C激活物,LPS组腹腔注射LPS(10 mg/kg,4 h)的方法建立败血症休克的实验动物模型,在建立败血症的实验动物模型的基础上,尾静脉注射PCA(0.4 mg/kg)为LPS+PCA组,每只大鼠均于药后30 min时运用Medlab生物信号采集处理系统记录平均动脉压(MAP)和左心室功能指标,并测定心肌中乳酸脱氢酶(LDH)活性、诱导性一氧化氮合酶(i NOS)活性及心肌病理切片。结果:PCA能明显减轻LPS诱导的心功能受损,并抑制心肌LDH的释放和i NOS活性的升高(P<0.05)。结论:PCA对败血症大鼠心脏血流动力学有明显的改善作用,其机制可能与通过保护血管内皮功能,改善微循环,稳定心肌酶活性和膜相结构等途径有关。
Objective:To investigate the effect of protein C activator from Agkistrodon halys venom on cardiac heinodynamics in septic shock rats. Methods: Twenty-four male SD rats were randomly divided into normal control (NC, n = 6), protein C activator (PCA, n = 6), lipopolysaecharide ( LPS, n = 6 ) and LPS + PCA group ( n = 6 ). NC group were given normal saline and PCA group were injected protein C activator (0.4 mg/kg) through vein of the tail. LPS group were administered lipopolysaccharide (10 mg/kg,4 h) by intraperitoneal injection method to make the model of septic shock rats. After the animal model was made,LPS+ PCA group were injected protein C activator (0.4 mg/ kg) through vein of the tail. 30 minutes after the injection,each rat was tested by Medlab biosignal analyzing system for observing mean arterial pressure and left ventricle function, the activity of LDH and iNOS in myocardiuin and the cuttings of myocardial tissues. Results : PCA could significantly attenuate cardiac function of rat in vivo induced by lipopolysaccharide and decrease the activities of LDH (P〈 0.01 ) and iNOS in myocardiuIn ( P 〈 0.05 ). Conclusion : PCA can evidently improve cardiac hemodynamics of the experimental animals. The mechanism may be resulted from the protection of blood vessel endotheliuin, improvement of microcirculation, stability of enzyme activity in myocardiuln or specific lnyocardial structure.
出处
《皖南医学院学报》
CAS
2007年第4期247-249,256,共4页
Journal of Wannan Medical College
基金
安徽省高等学校自然科学研究基金项目(2005KJ295
KJ2007B022)
关键词
蝮蛇毒
蛋白C激活物
内毒素
心脏血流动力学
心功能
实验研究
败血症
Agkistrodon venom
protein C activator
lipopolysaccharide
cardiac hemodynamics
cardiac function
experimental study