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对离体左,右心房肌,胺碘酮(Ami)1～100μmol·L~(-1)均有负性肌力作用,30μmol·L~1明显抑制心肌静息后收缩,正阶梯和成对刺激效应,1～10μmol·L~1使苯福林,异丙肾上腺素,组胺和CaCl_2正性肌力作用的量效曲线呈非竞争性拮抗作用,心肌动作电位和收缩力同步记录发现,Ami 30μmol·L~1减弱心肌收缩,延长APD,但对平台期和V_(max)无影响.故Ami的负性肌力作用可能是抑制心肌细胞外Ca~(2+)内流和细胞内Ca~(2+)释放所致,并非选择性阻滞心肌α,β和H_2受体以及电压依赖性钙通道引起 .
In isolated left and right atrial muscles, amiodarone (Ami) 1 ~ 100μmol·L ~ (-1) had negative inotropic effect, 30μmol·L ~ 1 significantly inhibited the contraction of myocardial resting, is the ladder and into The stimulation effect, 1 ~ 10μmol·L ~ 1 phenylephrine, isoproterenol, histamine and CaCl 2 positive inotropic effect showed a non-competitive antagonistic effect curve, synchronous recording of myocardial action potential and contractility , Ami 30μmol·L ~ 1 attenuated myocardial contractility and prolonged APD, but had no effect on the plateau phase and V max, so the negative inotropic effect of Ami may be the inhibition of extracellular Ca 2+ influx and cell Ca2 + release is not caused by selective block of myocardial α, β and H_2 receptors and voltage-dependent calcium channels.