Erythropoietin (EPO) protects the myocardium from ischaemic injury and promotes 
beneficial remodelling. We assessed the therapeutic efficacy of intracardiac EPO 
injection and EPO-mediated stem cell homing in a rat myocardial infarction (MI) 
model. Following MI, EPO (3000 U/kg) or saline was delivered by intracardiac 
injection. Compared to myocardial infarction control group (MIC), EPO 
significantly improved left ventricular function (n =11-14, P < 0.05) and 
decreased right ventricular wall stress (n = 8, P < 0.05) assessed by 
pressure-volume loops after 6 weeks. MI-EPO hearts exhibited smaller infarction 
size (20.1 +/- 1.1% versus 27.8 +/- 1.2%; n = 6-8, P < 0.001) and greater 
capillary density (338.5 +/- 14.7 versus 259.8 +/- 9.2 vessels per mm2; n = 6-8, 
P < 0.001) than MIC hearts. Direct EPO injection reduced post-MI myocardial 
apoptosis by approximately 41% (0.27 +/- 0.03% versus 0.42 +/- 0.03%; n = 6, P= 
0.005). The chemoattractant SDF-1 was up-regulated significantly assessed by 
quantitative realtime PCR and immunohistology. c-Kit(+) and CD34(+) stem cells 
were significantly more numerous in MI-EPO than in MIC at 24 hrs in peripheral 
blood (n = 7, P < 0.05) and 48 hrs in the infarcted hearts (n = 6, P < 0.001). 
Further, the mRNAs of Akt, eNOS and EPO receptor were significantly enhanced in 
MI-EPO hearts (n = 7, P < 0.05). Intracardiac EPO injection restores myocardial 
functions following MI, which may attribute to the improved early recruitment of 
c-Kit(+) and CD34(+) stem cells via the enhanced expression of chemoattractant 
SDF-1.