The effect of antiarrhythmic drugs on life-threatening XXXX induced by the interaction between acute @entity741 and sympathetic hyperactivity.

@entity1 @entity1169 @entity2643 @entity1165 @entity943 @entity1855 @entity2683 @entity3303 @entity1188 @entity741 @entity3159 @entity468 @entity204 @entity2779
Transient @entity741 , with attendant sympathetic hyperactivity, seems to play a major role in sudden @entity204 among @entity1 with @entity741 . @entity1165 ( @entity1165 ) and fibrillation (VF) are consistently and repeatedly elicited in @entity468 by the interaction between a 2-minute occlusion of the left descending coronary artery and a 30-second stimulation of the left stellate ganglion. When three consecutive trials yield almost identical results, time alone will not modify the response and a given drug can be injected to test its efficacy with an internal control analysis. In 90 @entity468 the efficacy of the following drugs was assessed: @entity3303 (n = 11), @entity2683 (n = 12), @entity2779 (n = 12), @entity1169 (n = 19), @entity3159 (n = 10), @entity2643 (n = 14), and @entity1855 (n = 12). Class I antiarrhythmic drugs completely failed to afford protection and worsening of @entity943 was observed in several instances. @entity1169 and @entity3159 showed efficacy in approximately 80% and 60% of the animals, respectively. @entity2643 and @entity1855 completely prevented the onset of @entity1165 and VF. Protection from @entity943 seems to be related to the combined presence of a noncompetitive adrenergic blockade associated with salutary effects on coronary circulation. These findings correlate with and help to explain the results of clinical trials in @entity1188 @entity1 . This model may help to provide a rational choice of antiarrhythmic drugs to be tested in clinical trials.
