Characteristics of early afterdepolarization in mouse atrial fibers.

Early afterdepolarization (EAD) in mouse atrial fibers was investigated under the treatment with aconitine, 3.0 mmol/L K+, quinidine, ryanodine or Bay k 8644. All of these EADs possessed the following common characteristics: all the parameters of EAD showed cycle length-dependence; take-off potential of the first triggered burst played an important role in the generation of the other parameters; hyperpolarization of the triggered brust enhanced the end of EAD; and the second plateau response might be used as an indicator of the capability of EAD generation of myocardiac cell. All those EADs were inhibited or abolished by nifedipine, tetrodotoxin or lidocaine. Potassium channel activators, lemakalim, thalium ion, acetyl-choline or high potassium could also inhibit or abolish the EADs. It is suggested that the EADs induced by different agents may base on a common mechanism: all currents contributing to the plateau phase of the action potential play an important role in the generation of EAD.