小鼠柯萨奇B_3病毒性心肌炎急性期心肌收缩力的改变及芪芩号对其影响

目的:观察小鼠柯萨奇B3(CVB3)病毒性心肌炎(VM C)急性期心肌收缩力的改变、采用并观察芪芩Ⅰ号(Q iq inⅠ)对CVB3-VM C小鼠心脏泵功能的改善。方法:采用BALB/C鼠建立CVB3病毒性心肌炎的动物模型,分为治疗组、病毒组和正常组,观察对比各组病变小鼠的一般情况、心脏收缩力指标LVP和LV dp/dtm ax变化、光镜下病理积分及电镜下心肌超微结构的改变。结果:病毒组第5、7天LVP和LV dp/dtm ax两指标均明显下降,与正常组比较有极显著性差异(P<0.01)。治疗组至第7天两指标均开始下降,低于正常组;与病毒组相比较,其LVP在第5、7天升高(P<0.05),LV dp/dtm ax在各时间点均有增高(P<0.01)。光镜下治疗组的心肌病理积分在第3~7天均低于病毒组(P<0.01)。电镜下可见病毒组小鼠心肌细胞线粒体肿胀、嵴断裂,肌丝溶解,肌浆网扩张,并在其中发现有病毒样颗粒;治疗组病变程度轻。结论:在急性期CVB3-VM C小鼠的心肌收缩力明显下降,与病毒直接损伤心肌,线粒体受损、大量心肌炎症坏死有关。芪芩Ⅰ号能明显减轻心肌的病理损害,提高CVB3-VM C小鼠的心肌收缩力。

The alteration of myocardial contractility in the acute phase of Coxsackievirus B_3 viral myocarditis in mice and the effect of QiqinⅠon it

Objective:To observe the alteration of myocardial contractility in the acute phase of Coxsackievirus B_3 viral myocarditis in mice,and the effect of QiqinⅠfor the pump function of heart on CVB_3-VMC in mice.Methods: CVB_3-VMC BALB/C mice were divided into treated group,virus group and control group.then the viabilities and the changes of LVP and LVdp/dtmax,pathological changes under light microscope and electron microscope and myocardial pathological scores of CVB_3-VMC mice of different groups were recorded.Results:Conpared with control group both LVP and LVdp/dtmax of virus group decreased significantly at the 5th day and 7th day(P<0.01),and in treat group LVP and LVdp/dtmax decreased significantly at the 7th day.Compared with virus group,LVP and LVdp/dtmax of treated group increased significantly at different time point(P<0.05).In myocardium of virus group under electron microscope,the infiltrating cells and the lysosomes in macrophagecytes and in cadiocytes were founded;mitochondria swelling,mitochondrial crista rupture,sarcoplasmic reticulum dilatation and virus-like particle in sarcoplasmic reticulum.But the changes of treated group were lighter.Conclusion: The LVP and LVdp/dtmax of CVB_3-VMC BALB/C mice decreased significantly in acute phase is relatedwith viral myocardial leision,the damage of mitochondria cadiocytes.QiqinⅠnot only could relieve myocardial histopathologic changes but also could improve cardiac hemodynamics in VMC mice.