Beta3-adrenoceptor activation just says NO to myocardial reperfusion injury.

For the increasing number of patients who survive an acute myocardial infarction, infarct size is the main determinant of further prognosis (1). Timely reperfusion is mandatory to reduce infarct size, and for all conditioning strategies— ischemic pre-conditioning, delayed ischemic pre-conditioning, ischemic post-conditioning, and remote pre-conditioning— reperfusion is a prerequisite to reduce infarct size (i.e., they delay rather than ultimately prevent infarct development) (2). he pioneering experiments demonstrating reduction of inarct size by timely reperfusion are only 40 years old (3), and nfarct size reduction by a variety of experimental interventions mmediately became an attractive target then (4). However, the nitial enthusiasm for all sorts of interventions to reduce infarct ize soon gave way to a more sober and critical view (5). In ontrast, infarct size reduction by reperfusion through thromolysis initially and primary percutaneous intervention subseuently was quickly translated to clinical use in patients with cute myocardial infarction (2).