The Study Of Effects Of Tashinone ⅡA-sulfoacid-natrum Injection On Electrical Activity Divorce Between Endocardium And Epicardium Induced By Myocardial Ischemia And Lidocaine Of Rabbit Heart In Vivo

Objective: To establish the model of electrical activitydivorce between endocardium and epicardium（EAD） induced bymyocardial ischemia and lidocaine; To study the effects of Tashinone ⅡA-sulfoacid-natrum injection (TSN) on the EAD.Methods:1. Theelectrocardiogram of standard II leader (ECG) and surfaceelectrocardiogram of epicardium(sECG1) and surface electrocardiogramof endocardium (sECG2) of rabbit were recorded simultaneously in vivo.2. To establish the model of the EAD with pituitrin hypophysin andadrenaline and lidocaine.3. To observe the effects of TSN on EAD.Fifty New Zealand rabbits were randomly divided into five groupsequally:①Blank control group: To observe for30minutes continuouslyafter NaCl5ml/kg was injected;②TSN negative control group: Toobserve for30minutes after TSN2.5mg/kg was injected;③Model group:The pituitrin hypophysin2U/kg and adrenaline0.1mg/kg and lidocaine4.9mg/kg were injected;④TSN preconditioning group: After TSN2.5mg/kg was injected for10min, then, the treatment same with modelgroup;⑤TSN therapy group: TSN2.5mg/kg was injected after themodel was established. ECG and sECG1and sECG2were observedsimultaneously.4. Statistics analysis: All the experimental datum were expressed as the mean value±standard difference (x±s), and dealt withsoftware SPSS19.0,the mean values comparision used one-way ANOVA,the difference was considered significance when the p value was less than0.05.Results:1. The changes in heart rate and interval Compared theblank control group(283±25bpm) with TSN negative controlgroup(266±22bpm), there was no significant difference; There was asignificant difference between the blank control group and model group（233±41bpm）or TSN preconditioning group（227±29bpm）or TSNtherapy group（83±23bpm）;There was a significant difference betweenthe negative group and TSN preconditioning group or TSN therapy groupor the model group;There was no significant difference between themodel group and TSN preconditioning group; There was a significantdifference between the model group and TSN therapy group; There wasa significant difference between TSN therapy group and TSNpreconditioning group;Compared TSN therapy group interval（0.77±0.22s）with the blank control group（0.21±0.22s） and TSNnegative group（0.24±0.03s） and the model group（0.24±0.03s）and TSNpreconditioning group （0.27±0.03s）,there was a significantdifference;There was no significant difference between the control groupand TSN negative group or TSN preconditioning group or TSN therapygroup.2. The changes in conduction time from endocardium andepicardium Compared the blank control group（5.09±1.83ms）with TSNnegative group（6.17±2.24ms）, there was no significant difference; Compared the blank control group with the model group（38.12±30.9ms）, there was a significant difference; Compared theblank control group with TSN preconditioning group（9.09±3.57ms）,there was no significant difference; Compared the blank control groupwith TSN therapy group（20.05±7.56ms）, there was a significantdifference; There was a significant difference between the blank modelgroup and TSN therapy group or TSN negative group;There was nosignificant difference between TSN preconditioning group and TSNnegative group; There was a significant difference between TSN therapygroup and the model group.3.The changes in ventricular arrhythmiasThere was no arrhythmia in blank control group and TSN negativecontrol group. In model group, TSN preconditioning group and TSNtreatment group, there were several kinds of arrhythmias, includingventricular premature bea（tVPB）, ventricular tachycardia（VT）, voltagealternation（VA）,ventricular flutter（Vf）, ventricular fibrillation（VF）and EAD. All arrhythmias mentioned above were occurred in modelgroup and TSN therapy group, however，there was no EAD in TSNpreconditioning group.There was a significant difference between theduration of arrhythmia in TSN preconditioning group（127.5±109.9s）and the model group （474.6±447.47s）; There was no significantdifference between TSN preconditioning group and TSN therapy group（634.1±402.7s）.4.The incidence rate and duration and transformationof EAD The EAD showed different frequency and rhythm between endocardium and epicardium, and there was no relation between eachother. No EAD occurred in blank control group and TSN negative controlgroup and TSN preconditioning group. The incidence rate of EAD was50%in model group and40%in TSN therapy group. ECG issynchronous with sECG1in rhythm and frequency, however, the rhythmand frequency between endocardium and epicardium were separatedduring EAD. The duration of EAD in model group and TSN therapygroup were362.6.±259.56s and294.2±256.94s, there was no significantdifference between two groups. The four animals died after EAD inmodel group, and the other turned to multiple premature ventricularbeat.An animal died after EAD In TSN therapy group. Conculsions:1.The lidocaine could induce electric activity divorce between endocardiumand epicardium on the background of general myocardial ischemia andeffect of adrenalin.2. The rhythm and frequency in electrocardiogramwas same as surface electrocardiogram of epicardium, however, theendocardium and epicardium were different during electrical activitydivorce is a serious ventricular arrhythmia.3.TashinoneⅡ A-sulfoacid-natrum injection could enhance the electrical stability ofmyocardium by improving myocardial ischemia and accelerating theconduction between endocardium and epicardium, thus reducing theoccurrence and development of electrical activity divorce betweenendocardium and epicardium.