维拉帕米对CVB_3感染心肌细胞Ca^(2+)内流及CVB_3-RNA含量的影响  

Effect of Verapamil on Ca^(2+) Influx and CVB_3-RNA Replication in Cultured Neonatal Rat Heart Cells Infected with CVB_3

作　　者：郭棋[1] 彭天庆[1] 杨英珍[1] 顾全保[2] 赵剑星[2] 

机构地区：[1]上海医科大学中山医院 [2]中国科学院上海细胞生物学研究所

出　　处：《中国生化药物杂志》1996年第2期47-50,共4页Chinese Journal of Biochemical Pharmaceutics

基　　金：国家自然科学基金资助课题(39170359)

摘　　要：观察了维拉帕米(Verapamil,Ver)对感染柯萨奇B_3病毒(CVB_3)的大鼠培养心肌细胞Ca^(2+)内流及CVB_3-RNA复制的影响。结果发现在感染48h后,Ver对感染细胞及正常对照的Ca^(2+)内流均有显著的抑制作用(P<0.01);若在病毒感染同时加入Ver,经48h培养后,细胞中CVB_3-RNA含量显著高于病毒对照组(P<0.05)。提示钙拮抗剂(如Ver)可减少病毒感染引起的心肌Ca^(2+)内流增加,有可能减轻感染细胞的继发性Ca^(2+)损伤;但Ver会促进病毒RNA的复制,提示在急性病毒性心肌炎临床上用Ver治疗心律失常时宜慎重。The effect of verapmil(Ver)on Ca2+ influx across the myocardial plasma membrane and cox-sackie virus B3(CVB3)-RNA replication in cultured neonatal rat heart cells infected with CVB, was investigated. It was found that the Ca2+ influx could be inhibited significantly (P<0. 01) by Ver (1 umol/L)after infection of heart cells for 48 h. However, when the cultured heart cells infected with CVB3 and treated with Ver(1 umol/L and 10 nmol/L) at the same time for 48 h,the amounts of CVB3-RNA in myocytes were significantly higher than that in infected control group (P<0. 05). These phenomenon suggests that the increase of Ca2+ influx of cultured heart cells infected with CVB3 could be inhibited by some calcium antagonist e. g Ver at the early stage. On the other hand,Ver might accelerate viral replication in myocardium. Thus, although Ver could be benefit for decreasing the secondary Ca2+damages and improving the myocardial electric activity.it isn't a sensible choice for therapy in acute stage of virus infection with cardiac symptoms.

关 键 词：柯萨奇B3病毒 维拉帕米 钙内流 药理 

分 类 号：R972[医药卫生—药品] R925.2[医药卫生—药学]