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目的探讨自身免疫机制在鼠巨细胞病毒(MCMV)诱导BALB/c鼠心肌炎室性心律失常中的作用。方法将无病原体4周龄BALB/c鼠60只,随机分为实验组(36只)和对照组(24只);实验组腹腔注射MC-MVTCID50悬液,对照组腹腔注射3T3细胞裂解液;记录所有小鼠心电图,观察心肌病理及炎性因子表达情况,检测血清抗心脏β1受体自身抗体滴度,膜片钳观察抗β1受体抗体对心肌细胞动作电位(AP)及L型钙通道(ICa-L)电流的影响。结果实验组心肌炎发病率69.4%,表现为心肌细胞变性或灶性坏死,炎性因子白细胞介素-1β和肿瘤坏死因子-α蛋白阳性表达,血管周围大量炎症细胞浸润。实验组心律失常累计发生率达50%,第6周起该组血清抗β1受体抗体滴度显著增高(与对照组比,P<0.01),且心律失常发生亦增加。1∶100抗β1受体抗体使小鼠心室肌细胞APD50和APD90延长15.3%和5.8%,使ICa-L密度显著增加。结论MCMV可能通过诱导抗β1受体自身抗体产生,增加ICa-L电流导致室性心律失常发生。
Objective To investigate the role of autoimmunity in ventricular arrhythmia induced by murine cytomegalovirus (MCMV) in BALB / c mouse myocarditis. Methods Sixty-four BALB / c mice without pathogens were randomly divided into experimental group (36) and control group (24). The experimental group was intraperitoneally injected MC-MVTCID50 suspension, and the control group was intraperitoneally injected with 3T3 cell lysate. The electrocardiogram (ECG) of all mice was recorded to observe the pathological changes of myocardium and the expression of inflammatory cytokines. The titers of anti-cardiac β1 receptor autoantibodies in serum were measured. The effects of anti-β1 receptor antibodies on cardiomyocyte action potential (AP) and L-type calcium channel (ICa-L) current. Results The incidence of myocarditis in experimental group was 69.4%, which showed as cardiomyocyte degeneration or focal necrosis, positive expression of inflammatory cytokines interleukin - 1β and tumor necrosis factor - α protein, and a large number of inflammatory cell infiltration around blood vessels. The cumulative incidence of arrhythmia in the experimental group reached 50%. From the 6th week, the antibody titer of anti-β1 receptor in serum of the experimental group was significantly increased (P <0.01 compared with the control group), and arrhythmia was also increased. A 1: 100 anti-β1 receptor antibody prolonged the APD50 and APD90 of mouse ventricular myocytes by 15.3% and 5.8%, resulting in a significant increase in ICa-L density. Conclusion MCMV may induce the occurrence of ventricular arrhythmia by increasing the ICa-L current induced by anti-β1 receptor autoantibodies.