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Despite elegant studies describing the phenomenon of RIRR in isolated myocytes, its biophysical properties and functional consequences in intact myocardium remain unclear. Here, we use ROS imaging to extend the concept of RIRR to the level of the intact heart. We establish regenerative superoxide production as the mediator of RIRR\u2010related arrhythmias and reveal their strong dependence on a key mitochondrial channel, known as the inner membrane anion channel (IMAC). We demonstrate the efficacy of suppressing RIRR and related arrhythmias either by pharmacologically blocking IMAC or scavenging ROS using a synthetic superoxide dismutase\/catalase mimetic.<\/jats:p>","DOI":"10.1113\/jphysiol.2011.214239","type":"journal-article","created":{"date-parts":[[2011,8,9]],"date-time":"2011-08-09T05:46:18Z","timestamp":1312868778000},"page":"5167-5179","source":"Crossref","is-referenced-by-count":54,"title":["Biophysical properties and functional consequences of reactive oxygen species (ROS)\u2010induced ROS release in intact 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