血必净注射液对心肺复苏后大鼠心肌肌钙蛋白T、心肌细胞Ca2+水平的影响

目的探讨血必净注射液对大鼠心肺复苏后心肌肌钙蛋白T(cTnT)、心肌细胞Ca2+水平及心肌病理改变的影响。方法建立心肺复苏大鼠模型,并将其随机分为3组,假手术组(大鼠在麻醉后仅行气管切开插管、颈动脉血管穿刺,而不进行窒息及心肺复苏试验,n=6)、模型组(大鼠在心肺复苏即刻通过尾静脉缓慢注射生理盐水4mL/kg,n=6)、血必净组(大鼠在心肺复苏即刻通过尾静脉缓慢注射血必净注射液4mL/kg,n=6)。检测心肺复苏前、后各组cTnT值、Ca2+荧光强度平均值及心肌病理变化。结果心肺复苏后6h,模型组、血必净组大鼠心肌细胞Ca2+荧光强度平均值高于假手术组(P<0.01)。与心肺复苏前比较,心肺复苏后6h模型组、血必净组大鼠的cTnT值均明显升高(P<0.01),尤以模型组升高幅度最大。血必净组大鼠心肌损害较模型组轻。结论血必净注射液可通过抑制心肌细胞钙超载,下调cTnT水平而发挥保护心肌的作用。

Effects of Xuebijing injection on levels of cardiac troponin T and Ca2+ in cardiac myocytes of rats after cardio-pulmonary resuscitation

Objective To investigate the effects of Xuebijing injection on levels of cardiac troponin T(cTnT),Ca2+ and pathological changes in cardiocytes of rats after cardiopulmonary resuscitation.Methods Rat models of cardiopulmonary resuscitation were established and randomly divided into 3 groups: sham operation group(tracheostomy and carotid artery puncture were performed after anesthesia without asphyxia and cardiopulmonary resuscitation test,n=6),model group(physical saline 4 mL/kg was injected slowly into the tail vein at the time of cardiopulmonary resuscitation,n=6) and Xuebijing group(Xuebijing injection 4 mL/kg was injected slowly into the tail vein at the time of cardiopulmonary resuscitation,n=6).The value of cTnT,average of Ca2+ fluorescence intensity and pathological changes of cardiocytes in each group before and after cardiopulmonary resuscitation were detected.Results 6 hours after cardiopulmonary resuscitation,average of Ca2+ fluorescence intensity in cardiocytes of rats in model group and Xuebijing group were higher than those in sham operation group(P<0.01).Compared with cardiopulmonary resuscitation before,cTnT values of rats in model group and Xuebijing group 6 hours after cardiopulmonary resuscitation were markedly increased(P<0.01),especially in model group increased the sharpest.Myocardial lesion of rats in Xuebijing group was slighter than that in model group.Conclusion Xuebijing injection plays the role of myocardial protection through inhibition of calcium overload and reduction of cTnT level in cardiocytes.