Ca2+Ca2+signal(itwas)regulatestheintracellularmanyimportantfunction,includingcellelectricexcited,andparticipateinmusclecontraction,vesiclessecretion,celltranscription,proliferationanddifferentiation,anddeath.Differentcellcalciumsignaltoreactdifferently,inthesamecell,thedifferentformsofcalciumsignalcanproducedifferentreaction.Forexampleinthemyocardialcells,actionpotentialCa2+tointernalflowtriggeringcellcontraction,Whileinpathophysiologicalconditions(e.g.myocardialhypertrophy),calciumsignalscanbeactivatedbygeneexpressiontranscriptionfactor,inductionofmyocardialphenotypereconstruction.Ofmyocardialcells,cells,calciumionsintheexcited(namelyactionpotential)andcellcontractionconnected,thisisforexcited-contractioncoupling(excitation-contractioncoupling,ECC).InECCprocess,myocardialcellexcitingcausecellmembranevoltagedependenceL-typecalciumchannelopenCa2+,exocellularinternalflow,withcalciuminductionCa2+-calciumrelease(Ca2+release,inducedCICR)ofthewaycausemyocardialcellmusclesarcoplasmicreticulum,slurrynets(SR)inashorttimethroughthemembraneofcalciumreleasechannel(namelyryanodinereceptor)tothecytoplasmandreleasealotofcalcium,causingthecytoplasmcalciumionconcentrationincreases,theinstantaneousnamelyforcalciumtransientsCa2+transient().Calciumtransientsthroughmusclecalciumprotein(troponin)causecellstocontract[1].Throughtheobservationofcalciumtransients,canunderstandmyocardialcellfunctionactivecharacteristicsandstatus.Therefore,webygivingdifferentconcentrationsofdrugperfusioneffectonventricularmusclecells,withlocalfieldelectricalstimulationofthewholecellcalciummethodinducedrelease(calciumtransients),observedifferentconcentrationsofdrugsoncardiacentricularmyocyteintracellularcalciumsignalinfluence,anditshappeningmechanismarediscussedforclinicalcardioasculardiseasepreventionprovidecertaintheoreticalbasis.