title: Erythropoietin is equally effective as fresh-blood transfusion at reducing infarct size in anemic rats.
abstract: OBJECTIVE
  We recently demonstrated that transfusion of anemic animals up to 100 g/L hemoglobin with fresh blood protects the heart from ischemic injuries following myocardial infarction. Erythropoietin has cardioprotective effects independent of its erythropoietic activity. The objective of this study was to compare the cardioprotective effects of erythropoietin treatment to fresh-blood transfusion in anemic rats after acute myocardial infarction.
  
  
  METHODS
  Randomized animal study.
  
  
  METHODS
  University laboratory.
  
  
  METHODS
  Male Sprague-Dawley rats weighing 200-300 g.
  
  
  METHODS
  Myocardial infarction was induced by coronary artery ligation in 76 rats, 55 of which were anemic (80-90 g/L) and 21 of which had normal hemoglobin levels. Animals were randomized to erythropoietin (2000 units/kg), fresh-blood transfusion to 100 g/L hemoglobin, or saline-treatment groups immediately following myocardial infarction.
  
  
  RESULTS
  At 24 hrs after myocardial infarction, cardiac function and infarct size were determined. Myocardial apoptosis was determined by caspase-3 activity and terminal deoxynucleotidyl transferase d-UTP nick end labeling (TUNEL) assay. Infarct size was significantly decreased in anemic rats treated with erythropoietin or blood transfusion compared to those in the saline-treatment group. Cardiac function, as measured by maximal positive and minimal negative first derivatives of left ventricular pressure, was better preserved in the normal hemoglobin groups and the erythropoietin- or transfusion-treated anemic animals compared to saline-treated anemic animals. Myocardial caspase-3 activity and TUNEL-positive nuclei were significantly increased in anemic rats but were decreased by erythropoietin treatment or red blood cell transfusion.
  
  
  CONCLUSIONS
  Erythropoietin treatment is equally effective as fresh-blood transfusion in anemic rats after acute myocardial infarction at reducing infarct size, myocardial apoptosis, and improving cardiac function.
authors.affiliation: Centre for Critical Illness, Research Lawson Health Research Institute, Canadian Blood Services, Ontario, Canada.
authors.forename: Anargyros
authors.initials: A
authors.lastname: Xenocostas
authors.forename: Houxiang
authors.initials: H
authors.lastname: Hu
authors.forename: Nicolas
authors.initials: N
authors.lastname: Chin-Yee
authors.forename: Xiangru
authors.initials: X
authors.lastname: Lu
authors.forename: Ian
authors.initials: I
authors.lastname: Chin-Yee
authors.forename: Qingping
authors.initials: Q
authors.lastname: Feng
mesh_terms: D000740:Anemia / Q000150:complications* / Q000188:drug therapy / Q000628:therapy; D000818:Animals; D017209:Apoptosis; D001794:Blood Pressure / Q000502:physiology; D001803:Blood Transfusion; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D053148:Caspase 3 / Q000378:metabolism; D004921:Erythropoietin / Q000627:therapeutic use*; D006321:Heart / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology; D006454:Hemoglobins / Q000032:analysis; D020287:In Situ Nick-End Labeling; D008297:Male; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy; D009206:Myocardium / Q000201:enzymology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D002316:Cardiotonic Agents; D006454:Hemoglobins; D004921:Erythropoietin; D053148:Caspase 3