胺碘酮对低O_2、酸中毒及肾上腺素条件下豚鼠左心室流出道自律细胞电活动的影响

Electrophysiological effects of amiodarone on pacemaker cells in guineapig left ventricular outflow tract under conditions of hypoxia,acidosis and treatment with epinephrine

目的:研究胺碘酮对豚鼠左心室流出道自律细胞电活动的影响以及胺碘酮对低O2、酸中毒和肾上腺素(EPI)所致该部位自律性改变的影响。方法:采用标准玻璃微电极细胞内电位记录技术,分别观测胺碘酮对豚鼠左心室流出道自发慢反应电位的影响,以及胺碘酮对无糖低氧、pH6.8和EPI导致的该电位改变的影响。结果:(1)0.1μmol/L胺碘酮可使左心室流出道自发慢反应电位自发放电频率(RPF)减慢,最大舒张电位(MDP)绝对值减小,复极80%时间(APD80)延长(P<0.05);1μmol/L胺碘酮可引起4相自动除极速度(VDD)和0相最大除极速度(Vmax)减慢,动作电位幅度(APA)减小,复极50%时间(APD50)延长(P<0.05),RPF减慢,MDP减小和APD80延长(P<0.01);10μmol/L胺碘酮可使VDD进一步减慢,APA进一步减小(P<0.01),其它指标的改变维持1μmol/L胺碘酮灌流时的水平。(2)低O2可使VDD、RPF和Vmax减慢,MDP和APA减小,APD50缩短(P<0.05);和低O2组相比,1μmol/L胺碘酮+低O2可使RPF和Vmax进一步减慢,MDP增大,APD80延长(P<0.05),VDD进一步减慢,APD50延长(P<0.01)。(3)pH6.8的灌流液可使VDD和RPF减慢,APD80缩短(P<0.05),Vmax减慢,APA减小(P<0.01);与pH6.8组相比,pH6.8的1μmol/L胺碘酮可使RPF进一步减慢,MDP和APA进一步减小,APD80延长(P<0.05),VDD进一步减慢,APD50延长(P<0.01)。(4)10μmol/LEPI可使VDD、RPF和Vmax加快,MDP增大,APD50和APD80缩短(P<0.05),APA增大(P<0.01);1μmol/L胺碘酮+10μmol/LEPI可使VDD和RPF减慢,MDP和APA减小,Vmax减慢,APD50和APD80延长(P<0.05,P<0.01)。结论:胺碘酮可降低豚鼠左心室流出道的自律性,同时对低O2、酸中毒和EPI所致的该部位自律性改变有一定的影响。

AIM ： To study the electrophysiological effects of amiodarone on the pacemaker cells in guinea - pig left ventricular outflow tract under the conditions of hypoxia, acidosis and treatment with epinephrine. METHODS ： The action potentials of the pacemaker cells in guinea - pig left vcntricular outflow tract were recorded by conventional intracellular microelectrode technique. The effects of amiodarone on the spontaneous slow response potentials were investigated under the conditions of hypoxia, acidosis and treatment with epinephrine. RESULTS： （ 1 ） Amiodarone at concentration of 0. 1μmol/L markedly decreased the rate of pacemaker firing （RPF） and maximal diastolic potential （ MDP）, lengthened 80% of the duration of action potential （ APD80 ）. Amiodarone at concentration of 1 μmol/L significantly decreased the velocity of diastolic depolarization （VDD） and RPF, the maximal rate of depolarization （Vmax）, MDP and amplitude of action potential （APA）, lengthened 50% of the duration of action potential （APD80） and APD80. Amiodarone at concentration of 10μmol/L led to a significant decrease in VDD and RPF, Vmax, MDP and APA, a notable lengthening in APD80 and APD80 was also observed. （2） Under the condition of hypoxia and perfusion with deprived glucose content for 15 min, VDD, RPF, MDP, Vmax and APA decreased significantly, APD80 was shortened notably. Under the condition of hypoxia, amiodarone at concentration of 1 μmol/L significantly decreased VDD, RPF and Vmax, increased MDP, lengthened APD80 and APD80 as compared to the cells treated with hypoxia only. （3） Perfusion with pH 6.8 solution for 10 min, VDD and RPF significantly decreased, Vmax and APA notably reduced, APD80 was markedly shortened. Under the condition of acidosis for 10 min, amiodarone significantly decreased VDD, RPF, MDP and APA, lengthened APDso and APD80 as compared to the cells under the condition of acidosis only. （4） Perfusion of epinephrine at concentration of 10 μmol/L for 10 min resulted in a significant increase in VDD, RPF, Vmax, MDP and APA, a notable shorting in APDso and APDs0 was also observed. Compared to 10 μmol/L epinephrine group, 1μmol/L amiodarone ＋ 10 μmol/L epinephrine significantly reduced VDD, RPF, Vmax, MDP and APA, lengthened APD50 and APD80. CONCLUSION： Amiodarone markedly decreases the autorhythmicity of the pacemaker cells in guinea - pig left ventricular outflow tract. This electrophysiological effects were significantly influenced by hypoxia, acidosis and epinephrine.