抗心律失常药对豚鼠左心室流出道自律细胞电活动的影响

目的:研究抗心律失常药对豚鼠左心室流出道自律细胞电活动的影响。方法:采用标准玻璃微电极细胞内记录技术,记录并分析了四类抗心律失常药及腺苷对离体豚鼠左心室流出道自发慢反应电位的效应。结果:ⅠA类抗心律失常药1μmol/L奎尼丁可使左心室流出道自发慢反应电位的放电频率(RPF)和4相自动去极速度(VDD)减慢(P0.05),动作电位幅度(APA)降低(P0.05),0相最大去极速度(Vmax)减慢(P0.05),复极50%(APD50)和90%时间(APD90)延长(P0.05);ⅠB类抗心律失常药1μmol/L利多卡因灌流标本后,RPF和VDD减慢(P0.05),最大复极电位(MDP)绝对值和APA减小(P0.05),Vmax减慢(P0.05),APD50和APD90缩短(P0.05);ⅠC类抗心律失常药0.5μmol/L普罗帕酮可使RPF(P0.01)和VDD(P0.05)减慢,APA降低(P0.05),Vmax减慢(P0.01),APD50(P0.01)和APD90(P0.05)延长;Ⅱ类抗心律失常药5μmol/L普萘洛尔可使RPF和VDD减慢(P0.01),MDP绝对值和APA减小(P0.01),Vmax减慢(P0.05),APD50和APD90延长(P0.01);Ⅲ类抗心律失常药1μmol/L胺碘酮可使RPF和VDD减慢(P0.01),APA降低(P0.01),Vmax减慢(P0.05),APD50(P0.01)和APD90(P0.05)延长;Ⅳ类抗心律失常药1μmol/L维拉帕米可使RPF和VDD减慢(P0.01),MDP绝对值和APA减小(P0.05),Vmax减慢(P0.05),APD50和APD90延长(P0.05);50μmol/L腺苷可使RPF和VDD减慢(P0.05),APA降低(P0.05),Vmax减慢(P0.01),APD50和APD90缩短(P0.05)。结论:抗心律失常药均可显著降低左心室流出道组织的自律性,通过改变APD50和APD90影响有效不应期而起到抗心律失常作用。

Electrophysiological effects of antiarrhythmic drugs on pacemaker cells in guinea pig left ventricular outflow tract

Objective： To explore the electrophysiological effects of antiarrhythmic drugs on pacemaker cells of left ventricular outflow tract. Methods： By using conventional intracellular microelectrode technique to record action potentials, series antiarrhythmic chugs were used to investigate the electrophysiological features and regularities of spontaneous activity of left ventricular outflow tract. Results： （1） Perfusion with 1 μmol/L quinidine resulted in a significant decrease in rate of pacemaker firing（ RPF, P 〈 0.05）, velocity of diastolic depolarization （ VDD, P 〈 0.05 ） , amplitude of action potential（ APA, P 〈 0.05 ）, and maximal rate of depolarization（ V P 〈 0.05 ）, and a marked proloning in 50% and 90% of duration of action potential（APD50 and APDgo, P 〈 0.05）. （2）1μmol/L lidocaine decreased RPF, VDD, MDP, APA and Vmax significantly （ P 〈 0.05）, shortened APD50 and APD90 notably（ P 〈 0.05）. （3）1 μmol/L propafenone led to a significant decrease in RPF（ P 〈 0.01 ）, V DD（ P 〈 0.05）, APA（ P 〈 0. 05 ）, Vmax （ P 〈 0.01 ）, and a marked prolonging in APD50 （ P 〈 0.01 ） and APD90 （ P 〈 0.05）. （4）Application of 5 μmol/L propranolol resulted in a significant decrease in RPF and VDD （ P 〈 0.01 ）, MDP and APA（ P 〈 0.01 ）, Vmax（ P 〈 0.05） and a notable prolonging in APD50 and APD90（ P 〈 0.05）. （5）Perfusion with 1 μmol/L amiodarone resulted in a significant decrease in RPF and VDD （ P 〈 0.01 ）, APA（ P 〈 0.01 ）, Vmax （ P 〈 0.05）, a marked prolonging in APD50 （ P 〈 0.01 ） and APD90 （ P 〈 0.05）. （6） 1μmol/L verapamil significantly decreased RPF and VDD （ P 〈 0.01 ）, MDP and APA （ P 〈 0.05）, Vmax（ P 〈 0.05）, notably prolonged APD5o and APDgo （ P 〈 0.01 ）. （7）50 μmol/L adenosine significantly decreased RPF and VDD （ P 〈 0.05 ）, APA（ P 〈 0.05 ）, Vmax（ P 〈 0.01 ）, markedly shortened APD50 and APD90 （ P 〈 0.05）. Conclusion： All kinds of antiarrhythmic drugs can decrease the autorhythmicity of guinea pig left ventricular outflow tract. By altering APD50 and APD90, they can affect effective refractory period（ERP） and having a significant effect on autorhythmicity of left ventricular outflow tract.