| Background:In recent years,despite the radiofrequency ablation,implantable cardioverter defibrillator(ICD)and other non-drug treatment of arrhythmia has made great progress,the drug is still the most important means of controlling arrhythmia.However,traditional antiarrhythmic drugs have antiarrhythmic effects in the treatment of arrhythmia.Therefore,the development of new antiarrhythmic drugs with small side effects is still the focus of research.More and more studies have found that late sodium current(INaL)plays an important role in maintaining the action potential plateau(stage 2),deciding the action potential duration(APD)and transmural dispersion of repolarization.The occurrence of arrhythmia is closely related to the abnormal increase of INaL In a variety of pathological conditions.INaL inhibitors have been shown to improve cardiac function and treat arrhythmias.The development of new inhibitors targeting INaL may provide more hope for treatment of arrhythmias,because of the low risk of arrhythmia induced by INaL inhibitors.Tannic acid,a polyphenolic compound,is an active ingredient of herbs commonly used in traditional Chinese medicine prescriptions.It can function as an antioxidant,antihemorrhagic,anticancer,or antihistaminic agent and prevent cerebrovascular diseases.Howere,the antiarrhythmic effects of tannic acid and its related mechanisms are rarely reported.Objective:To explore the effect of tannic acid on field action potential duration(FPdur)and excitation conduction velocity(ECV)in rabbit ventricular muscle in normal and heart failure using microelectrode arrays(MEA)technology.Explore the inhibitory effect of tannic acid on INaL,and to provide a theoretical basis for the development of new INaL inhibitors for clinical treatment of arrhythmia.Methods:Ninety-six adult New Zealand white rabbits were randomly divided into 12 groups:control group(n=8),tannic acid groups(10,30,50,and 80 μmol/L;n=8 for each concentration),ATX group(n=8),ATX+tannic acid groups(10,30,50,and 80 μmol/L;n=8 for each concentration),heart failure group(n=8),and heart failure+tannic acid group(80 μmol/L;n=8).The heart was perfused with modified Tyrode’s solution.Flexible electrodes were attached to the left ventricular muscle to record FPdur and ECV.Results:In the tannic acid(10,30,50,and 80 μmol/L)groups,FPdur decreased from 363.88±11.00 in the control group to 345.O0±9.52,329.13±8.41,313.75±10.02 ms,and 296.75±10.42ms,respectively,whereas ECV significantly increased from 0.56±0.05 to 0.63±0.04,0.69±0.03,0.76±0.04 m/s,and 0.84±0.05m/s,respectively.In the ATX group,FPdur increased from 363.88 ± 11.00 in the control group to 408.75± 10.82 ms(P<0.05).However,there was no significant change in ECV(P>0.05).In the ATX(10,30,50,and 80 μmol/L)groups,FPdur decreased from 408.75±10.82ms in ATX group to 376..00±11.82、341..38±11.82、319..50±11.82,and 301..63±11.82ms,respectively,whereas ECV significantly increased from 0.51±0.04m/s to 0.57±0.03、0.64±0.05、0.70±0.05,and 0.80±0.04m/s,respectively.The FPdur shortening effect in the ATX+tannic acid group was significantly stronger than that in the tannic acid group.In the heart failure group,FPdur increased from 363..88±11.00ms in the control group to 495.50±13.56ms,and ECV decreased from 0.56±0.05m/s to 0.43±0.05m/s(P<0.05).In the heart failure+tannic acid(80 μmol/L)group,FPdur decreased from 495.50±13.56ms in the heart failure group to 442.75±13.56ms,and ECV increased from 0.43±0.05m/s to 0.57±0.06m/s(P<0.05).Conclusion:1.MEA technology can reflect the ventricular electrophysiological characteristics quickly and accurately.2.Whether in normal or heart failure state,tannic acid can decrease FPdur and increase ECV in rabbit ventricular muscle in a concentration dependent manner.So that tannic acid might be effective inhibitors of INaL,and plays a unique role in antiarrhythmic therapy. |
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