@entity741 includes a number of entities that have been grouped in accordance with physiopathology and evolutive criteria. In recent years 'new' @entity63 have been described. Within the 'new' @entity63 , ventricular post- @entity63 dysfunction--also known as 'stunned @entity1562 '--is worth mentioning. In this route, several studies have suggested that reperfusion per se could cause cellular injury ( @entity5721 ). In previous years, a protective effect on the injury caused by @entity63 and reperfusion in the heart has been attributed to @entity859 . These effects have been documented in different experimental in vivo and in vitro models. Thus, the administration of exogenous @entity859 , or agonists of @entity859 receptors prior to @entity63 reduces the size of the @entity1188 , improves the recovery of the ventricular function during reperfusion (attenuating stunning) and prolongs the time period to the @entity5649 . However, focusing on a potential therapeutic application, it is of the utmost importance to find this protection and learn the mechanisms involved when procedures are applied during early reperfusion. We showed that @entity859 , administered from the beginning of reperfusion, attenuated systolic and diastolic (myocardial stiffness) alterations of the stunned @entity1562 . This protective effect was mediated by the activation of A1 @entity859 receptors, and without modification on infarct size. According to some authors, @entity859 can decrease the release of endothelin, during early reperfusion, and reduce an overload of @entity141 that could cause a cellular lesion. Finally, @entity63 preconditioning involves a series of intracellular events that are initiated with the activation of the A1 receptor, and end at the sensitive K+ @entity855 channels of the mitochondria. The phosphorylation and opening of these channels would cause the protective effect. Activation of this specific mechanism during reperfusion has not been studied extensively.

XXXX and cardioprotection during reperfusion--an overview.

@entity859 :: ('MESH:D000241', 'Chemical') :: ['adenosine'] @entity5721 :: ('MESH:D015427', 'Disease') :: ['reperfusion injury'] @entity5649 :: ('MESH:D054061', 'Disease') :: ['ischemic contracture'] @entity63 :: ('MESH:D007511', 'Disease') :: ['ischemia', 'ischemic', 'ischemic syndromes'] @entity1188 :: ('MESH:D007238', 'Disease') :: ['infarction'] @entity1562 :: ('MESH:D017682', 'Disease') :: ['myocardium'] @entity741 :: ('MESH:D017202', 'Disease') :: ['Ischemic heart disease'] @entity141 :: ('CHEBI:29108', 'Chemical') :: ['Ca2+'] @entity855 :: ('MESH:D000255', 'Chemical') :: ['ATP']
@entity859 :: (MESH:D000241,Chemical) :: ['Adenosine']
