902).

In the EPO group, there was a reduction in left ventricular end-systolic and end-diastolic diameters (LVESD and LVEDD, respectively), as compared to the control group. Conclusion: Our results indicated that perioperative exogenous EPO infusion could not improve the ventricular function and wall motion index in the immediate post-CABG weeks. Nevertheless, a reduction in LVEDD and LVESD at 4 days and 30 days after CABG in the EPO group, by comparison with the control group, suggested that EPO correlated with a reduction in the remodeling of myocytes and reperfusion injuries Inhibitors,research,lifescience,medical early after CABG. Trial Registration Number: 138809102799N1 Keywords: Erythropoietin, Ischemia, Reperfusion injury, selleck chemicals llc Coronary artery bypass graft Introduction Erythropoietin (EPO) is a glycoprotein hormone produced by the kidney and plays a key role in hematopoiesis.1

In addition to these hematopoietic effects, EPO exerts non-hematopoietic effects on some tissues like the brain,2 kidney,3 retina,4 and muscles.5 Inhibitors,research,lifescience,medical Moreover, both ventricular myocytes and endothelial cells have EPO receptors.6 EPO wields its protective effects on myocardial cells via different Inhibitors,research,lifescience,medical pathways, including stimulation of neovascularization, activation of the PI3K and 2.1 ERK pathways,7,8 and synthesis stimulation of endothelial progenitor cells from the bone marrow.9,10 Coronary artery bypass graft surgery (CABG), an Inhibitors,research,lifescience,medical important treatment modality in ischemic patients, increases myocardial perfusion and ejection fraction (EF) in patients with coronary artery diseases.11 Although the rapid reperfusion by CABG significantly reduces mortality and morbidity,12 this reperfusion paradoxically may contribute to myocardial stunning injuries and/or death after CABG.13,14 Therefore, new treatment modalities should focus on decreasing damage after reperfusion. In addition to the protective effect of EPO on myocardial ischemia, studies on animal Inhibitors,research,lifescience,medical models have shown that EPO can also reduce reperfusion tissue injuries.15-17 Studies on human models have, however, proved somewhat controversial.18,19

While some authors have reported that EPO can reduce ischemia-reperfusion injuries in the myocardium and posited the possible mechanism for this action,20,21 others such as Mocini et al.19 in a different model, SB-3CT performed on patients having undergone CABG, have maintained that EPO has no association with a reduction in the levels of myocardial biomarkers (troponin I and CKMB) after CABG. The latter group of authors justify their conclusions by arguing that EPO induces tissue protection with anti-apoptotic mechanism. Nonetheless, these authors assessed the effects of EPO by two indicators of necrosis, namely troponin I and CKMB. The left ventricular (LV) function is usually described in terms of the EF.