What are the direct mechanisms involved? This question cannot be answered by the results of this study. In the case of sotalol we have found that increase in intercellular coupling is related to an increase in intracellular cAMP concentration ; thus, the same mechanisms may be involved even in the defibrillating effect of tedisamil. This possibility, the effect of tedisamil on free intracellular Ca2+ concentration and its effect on intercellular synchronization are under further investigation.
CONCLUSIONSOur results show a new property of tedisamil, ie, protection or enhancement of intercellular coupling, which can improve intercellular synchronization and thereby support spontaneous ventricular defibrillation. This new finding can elucidate the antiarrhythmic-defibrillating ability of te-disamil unrelated to its class III properties. It supports our previous hypothesis relating spontaneous defibrillation with sympathomimetic features, and underlines the cardioprotective effects of cAMP and catecholamines even in the case of class III antiarrhythmic drugs. It can lead to the development of a new clinically important antiarrhythmic-defibrillating compound.
ACKNOWLEDGEMENTS: We thank Dr N Tribulova, Institute for Heart Research, SAS, Bratislava, Slovakia, for her fruitful cooperation and constructive criticism.
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