Objective: The goal of this study is to observe the electrophysiological effect of adenosine triphosphate (ATP) on the normal heart or how it triggers activities of the mechanism of arrhythmias induced by ATP. Methods: A Franz 6F catheter was introduced into the left ventricle to record monophasic action potentials (MAPs) using the contact electrode technique to observe the influence to MAP change of normal heart and triggered activities with CsCl-induced when ATP is administered as an intravenous bolus.Results: On one hand ATP has little effects on the amplitude and the maximal upstroke velocity (Vmax) of MAP in the normal heart. But at first the heart rate doesn’t slows down appreciably and adenosine-induced early after- depolarization (EAD) that are associated with a prolongation the MAP duration (MAPD90)

and in the later period the heart rate clearly slows down and EAD disappears. On the other hand it has biphasic effect on delayed after depolarization (DAD) or EAD induced by CsCl. In the initial stage it promotes after depolarization (EAD or DAD) temporarily and then abolishes them quickly. Conclusion: The effect of ATP is variable in different heart states. It shows the biphasic effects of excitement and repression

and is related to dosage. This is important to the clinical use of ATP.