Carson D L, Dresel P E
J Cardiovasc Pharmacol. 1981 Sep-Oct;3(5):924-35. doi: 10.1097/00005344-198109000-00002.
The effect of lidocaine on the conduction of extrasystoles was studied in 8 open-chest dogs after atrioventricular nodal block. Simultaneous recording of endocardial and epicardial activation provided separate measures of endocardial (Purkinje) conduction as well as myocardial (muscle) conduction. Lidocaine (1.25--10.0 mg/kg) caused a dose-dependent slowing of conduction of midrange extrasystoles (250--400 ms) in both the Purkinje system and the myocardium, which became statistically significant at doses larger than 1.25 mg/kg. On the other hand, low doses of lidocaine caused speeding of early extrasystoles, i.e., coupling intervals (less than 250 ms) in the Purkinje system but not in the myocardium. Measurement of transmural conduction time as a function of coupling interval revealed a period of "apparent" supernormal conduction through ventricular muscle that was eliminated at high doses of lidocaine.
在8只开胸犬房室结阻滞模型上，研究了利多卡因对早搏传导的影响。同步记录心内膜和心外膜激动，分别测量心内膜（浦肯野纤维）传导和心肌（肌肉）传导。利多卡因（1.25-10.0mg/kg）可使浦肯野纤维系统和心肌中程早搏（250-400ms）的传导呈剂量依赖性减慢，剂量大于1.25mg/kg时具有统计学意义。另一方面，小剂量利多卡因可使早期早搏（即浦肯野纤维系统中耦联间期小于250ms）的传导加速，但对心肌无此作用。测量跨壁传导时间与耦联间期的关系发现，在高剂量利多卡因作用下，心室肌“表观”超常传导期消失。
