Experimental models of XXXX .

@entity1165 @entity1166 @entity235 @entity1168 @entity95 @entity5166 @entity1372 @entity972 @entity1162 @entity1371
@entity1166 is a potentially life threatening form of polymorphic @entity1165 typically seen in the setting of congenital and acquired @entity1162 . Numerous in vitro studies have investigated basic ionic mechanisms underlying delayed repolarization. The role of different ion channels and the induction of early afterdepolarizations have been studied in various cardiac cells including M cells. In addition, isolated heart models with and without electrical stimulation and/or the use of drugs which prolong repolarization have been developed in recent years. Some of these models have simulated conditions likely to exist in the clinical setting of @entity1166 , such as @entity1168 and @entity1371 . In in vivo @entity235 and @entity95 models, torsade-like polymorphic @entity1165 have been induced by the administration of different agents such as @entity5166 , neurotoxins, e.g., anthopleurin or various class III drugs under conditions designed to mimic the clinical situation. In the context of recent advances in the molecular genetics of @entity1162 , those models which have used @entity1372 or @entity972 channel blockers have gained particular interest. Based on all experimental studies it seems probable that the first beats of torsade occur due to early afterdepolarizations and triggered activity. The development of subsequent beats is less clear. Reentry based on inhomogeneity of refractoriness has been suggested as the underlying mechanism.
