The effect of verapamil on Ca2+ influx across the myocardial plasma membrane and coxsackie virus B3 （ CVB3）-RNA replication in cultured neonatal rat heart cells infected with CVB3 was investigated. It was found that the Ca2+ influx could be inhibited significantly （P<O. 01） by verapamil （1 μmol/L） after infection of heart cells for 48h. However

when the cultured heart cells infected with CVB3 and treated with verapamil （Iμmol/L and 10 nmo/L） at the same time for 48h

the amounts of CVB3-RNA in myocytes were significantly higher than that in infected control group （P<O. 05）. These phenomena suggest that the increase of Ca2+ influx of cultured heart cells infected with CVB3 could be inhibited by some calcium antagonists

e. g. verapamil at the early stage. On the other hand

verapamil might accelerate viral replication in myocardium. Thus

although verapamil could be beneficial for decreasing the secondary Ca2+ damages and improve the myocardial electric activity

it isn’t a sensible choice for therapy in early stage of virus infection with cardiac symptoms.