Central sympathetic activation and endothelin modulate ischemia-induced arrhythmogenesis, with endothelin impairing local conduction and central sympathetic activity partly counterbalancing this effect.
Does not support clonidine use post-MI; leaves open translation of rat autonomic-endothelin findings.
We investigated the effects of autonomic dysfunction and endothelin on local conduction and arrhythmogenesis during myocardial infarction. We recorded ventricular tachyarrhythmias, monophasic action potentials, and activation sequences in wild‐type and ET B ‐deficient rats displaying high endothelin levels. Central sympathetic inputs were examined after clonidine administration. Clonidine mitigated early and delayed arrhythmogenesis in ET B ‐deficient and wild‐type rats, respectively. The right ventricular activation delay increased in clonidine‐treated ET B ‐deficient rats and slightly decreased in wild‐type rats. The left ventricular voltage rise decreased in all groups, whereas the activation delay increased mainly in clonidine‐treated ET B ‐deficient rats. Central sympathetic activation and endothelin modulate ischemia‐induced arrhythmogenesis. Ischemia alters excitability, whereas endothelin impairs local conduction, an action partly counterbalanced by central sympathetic activity.
No takes yet. Share an insight, caveat, or question.
Kolettis et al. (2016) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: