Abstract
Aim: Acute myocardial infarction is a major cause of morbidity and mortality worldwide. Although thrombolytic therapy and primary percutaneous coronary intervention are the therapeutic approaches to reduce the myocardial ischemic injury and limit the infarct size by providing reperfusion, process can itself induce cardiomyocyte death known as myocardial reperfusion injury. In addition to effects on immunsuppression for organ transplantation, tacrolimus has diverse actions that result in amelioration of ischemia/reperfusion (I/R) injury. In this study, we aimed to evaluate the effects of tacrolimus on myocardial I/R injury in rats.
 Material and Methods: Adult male Wistar albino rats (n=18; mean weight, 252±20 g; age, 46-54 days) were included to this study. Rats were randomly assigned into three groups: Group 1 (sham, n=4), Group 2 (I/R+saline, control, n=7), Group 3 (tacrolimus+I/R, n=7). Tacrolimus (0.1 mg/kg) was administered as an intravenous infusion in the first 15 min of reperfusion after 45 min ischemia period. 
 Results: Although there were no change in area at risk, infarct size was markedly reduced in tacrolimus group when compared to control group (p
Highlights
Myocardial ischemia/reperfusion (I/R) injury leads to severe arrhythmias and associated with high risk of mortality [1]
Percutaneous coronary intervention (PCI) has a positive effect on survival of patients with acute myocardial infarction (AMI), there is evidence suggesting that percutaneous coronary intervention (PCI) increases the heart failure risk in patients with AMI, as it leads to myocardial I/R that result with myocardial injury and cardiomyocyte death [3]
We aimed to investigate the protective effect of tacrolimus on myocardial I/R injury in a rat model by using hemodynamical, histopathological, and biochemical evaluations
Summary
Myocardial ischemia/reperfusion (I/R) injury leads to severe arrhythmias and associated with high risk of mortality [1]. Inflammatory cascade is activated with reperfusion and cardiomyocyte death and apoptosis occur during this period. Tacrolimus, known as FK506, is a calcineurin inhibitor, and acts as an immunsuppresive agent It is used typically in organ transplantations to reduce the risk of graft rejection and autoimmune diseases [4]. Several studies have revealed that tacrolimus has an antioxidative and antiapoptotic effects [5] It blocks the catalytic activity of calcineurin and this leads to gene repression that regulates the production of adhesion molecules and cytokines. Due to this repression with tacrolimus, inflammatory cell response, platelet activation, neutrophil adhesion and aggregation decrease in I/R injury [6]
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