Antiarrhythmic peptides were described for the first time in 1980 by Aonuma and colleagues . These peptides were found to enhance synchronization in embryonic chick heart cell aggregates and to suppress aconitine and CaCl2-induced arrhythmias in mice in vivo. However, the mechanism of action remained unclear. After Argentieri and coworkers reported that the natural antiarrhythmic peptide did not directly influence action potential duration, upstroke velocity or resting membrane potential in isolated Purkinje fibre strands, this field was no longer a matter of debate, probably because at that time gap junctions and cellular coupling were not at the centre of interest, and cardiovascular pharmacology focused on the development of new sodium and potassium channel blockers as antiarrhythmic agents.In our experiments, we started to investigate the influence of natural and synthetic antiarrhythmic peptide using a mapping system allowing observation of the spread of activation and the distribution of electrophysiological parameters on the heart’s surface. Natural AAP and AAP10 reduced the epicardial dispersion of action potential duration, as shown. It is commonly accepted that a dispersion in action potential duration makes the hearts more susceptible to reentrant arrhythmia and thereby to ventricular fibrillation . It was shown in a previous study that AAP10 pretreatment reduced the ischemia-induced disturbance of the activation pattern and reduced the incidence of ventricular fibrillation. Best quality drugs cheap: find Xopenex Price here and discover best deals online.