The purpose of this study was to elucidate whether te-disamil affects intercellular coupling and whether this effect can explain, in a new way, its defibrillating ability. Tedisamil has class III antiarrhythmic properties, ie, it prolongs APD and effective refractory period (ERP), decreases heart rate and exhibits positive inotropic effects . Like other class III antiarrhythmic drugs with positive inotropic effects, te-disamil has been found to terminate VF in perfused heart in Langendorff preparation and to support spontaneous defibrillation in vivo (unpublished data). The antiarrhythmic defibrillating effects of class III antiarrhythmic compounds have been explained by the prolongation of APD and ERP. This explanation of class III defibrillating effect should be reexamined because many other compounds such as adrenaline, tricyclic antidepressants and phenothiazines exhibit clear defibrillating ability , although they shorten APD and ERP, and prolongation of APD does not always support spontaneous defibrillation.
On the basis of our hypothesis that spontaneous ventricular defibrillation requires a high degree of intercellular synchronization, we suggested that any drug could support the defibrillating ability of the heart if it enhances intercellular coupling, increases intracellular cAMP concentration and decreases intracellular free Ca2+ concentration, thereby preventing its decoupling effect.
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