Failure of erythropoietin to render jeopardized ischemic myocardium amenable to incremental salvage by early reperfusion.

摘要: OBJECTIVES Erythropoietin (EPO) has been thought to be capable of potentiating protection jeopardized myocardium by reperfusion in evolving myocardial infarction. However, diversity study design and measurements infarct size studies evaluating EPO led inconsistent results. We sought characterize the effect on after ischemia with use assessment left-ventricular (LV) creatine kinase (CK) depletion echocardiography. METHODS Acute coronary occlusion was induced 10-week-old C57BL6 mice left anterior descending artery ligation for 3 h followed 72 reperfusion. (10,000 U/kg) or an equivalent amount saline vehicle alone injected intraperitoneally before immediately onset Assays residual LV CK activity calculation were performed homogenates harvested measurement size, echocardiography harvest tissue function. RESULTS Mice administered had similar (37.1+/-4.1%) echo scores (22.9+/-0.4) compared those corresponding control (35.29+/-1.9 21.3+/-1.1%, respectively). (39.1+/-4.8%) (19.5+/-1.0) (40.3+/-4.9 21.5+/-1.9%, CONCLUSION does not protect ischemic such that can yield additional salvage.