心室流出道室性心动过速模型的构建

目的构建特发性流出道室性心动过速(简称室速)的动物模型。方法选择新西兰大白兔20只,随机分为室速组和对照组,每组10只。通过高频(50ms,5.0V)刺激心外膜主动脉与肺动脉交界处,导致室速的发生。实验结束后立即取出左右流出道心肌组织,采用免疫组化方法检测酪氨酸羟化酶染色阳性的交感神经纤维,观察其形态、分布及密度变化,其密度采用阳性纤维或结构在选区中的面积比表示。结果 10只兔6只诱发出流出道室速;室速组兔左、右流出道心室肌组织神经分布与对照组不同,其密度明显增高(P0.05)。结论心外膜主动脉与肺动脉交界处高频刺激可诱发流出道室速的发生。

The construction of rabbit models of idiopathic ventricular outflow tract tachycardia

Objective To construct the rabbit models of idiopathic ventricular outflow tract tachycardia. Methods The rabbits were randomly divided into two groups ： ventricular tachycardia （VT） group （ n = 10 ） and control group （ n = 10）. The rabbits were given high-frequency（50 ms,5.0 V） stimulation of sympathetic nerve at the epidium juncture of aor- ta and pulmonary artery to reduce ventricular outflow tract tachycardia. Myocardium were dislodge of left and fight ventricular outflow tract instantly after the rabbits death. Sympathetic nerve fibers which were tyrosine hydroxylase （TH） positive were detected by immunohistochemistry staining. The difference of morphology, disposition and density were observed. The density was represented by assignment area of positive nerve fibers or architecture. Results Six of ten rabbits in VT group were induced outflow tract VT . Compared to control group, the density of TH positive nerves was much higher from ventricular myocardium of left and fight ventricular outflow tract in VT group. Conclusion High-frequency stimulation of at the epidium juncture of aorta and pulmonary artery can induce outflow tract ventricular tachycardia.