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三丙酮胺(Triacetonamine-HC1,TAA)明显延长离体豚鼠心肌ERP(有效不应期),APD(动作电位时程)和ERP/APD_(90),使坪台水平略为下降,但不影响APA(动作电位幅度),V_(max)(零相最大去极速率)和RP(静息膜电位),TAA抑制心肌自发异位节律性和由Ba~(2+)式缺氧诱发的自律活动,延长LP(动作电位潜伏期),提高TS(阈刺激强度);用高钙液灌流心肌,可部分逆转TAA的作用;TAA显著抑制由高K~+造成的SRAP(慢反应动作电位),并呈电压及频率依赖性;TAA可逆转利多卡因和乙酰胆碱缩短APD的作用.结果提示TAA通过抑制自律性,延长不应期及阻滞Ca~(2+)内流而起抗心律失常的作用.
Triacetonamine-HC1 (TAA) significantly prolonged the ERP (effective refractory period), APD (action potential duration) and ERP / APD_ (90) in isolated guinea pigs, and decreased the level of Pingtai slightly, but did not affect APA (Action potential amplitude), V max (zero phase maximum depolarization rate) and RP (resting membrane potential), TAA inhibited spontaneous ectopic rhythm of myocardium and autonomic activity induced by Ba 2+ hypoxia , Prolonged LP (action potential latency) and increased TS (threshold stimulation intensity); TAA was partly reversed by perfusion of myocardium with high calcium; TAA significantly inhibited SRAP (slow response action potential) caused by high K + TAA reverses the effect of lidocaine and acetylcholine in shortening APD.The results suggest that TAA can prevent arrhythmia by inhibiting autonomic activity, prolonging refractory period and blocking Ca 2+ influx .