Myocardial protection by erythropoietin during resuscitation from ventricular fibrillation

Human recombinant erythropoietin (rhEPO) can protect the myocardium during ischemia and reperfusion. We investigated whether rhEPO could ameliorate previously identified functional myocardial abnormalities that develop during resuscitation from cardiac arrest, using a rat model of ventricular fibrillation (VF) and closed-chest resuscitation. VF was electrically induced and maintained, untreated, for 10 minutes. Chest compression and ventilation were then started and electrical defibrillation was attempted 8 minutes later. Rats were randomized to receive rhEPO (5000 U/kg) in the right atrium at baseline, 15 minutes before induction of VF (rhEPOBL -15-min), or at 10 minutes of VF, immediately before the start of chest compression (rhEPOVF 10-min), or to receive 0.9% NaCl solution instead (control). rhEPO given at the time of resuscitation (rhEPOVF 10-min group) -- but not at baseline -- prompted more effective chest compression, yielding higher coronary perfusion pressures for a given compression depth (1.95 +/- 0.27 mm Hg/mm; P < 0.05 in comparison with rhEPOBL -15-min [1.63 +/- 0.23 mm Hg/mm] and control [1.62 +/- 0.26 mm Hg/mm], by Dunnett's multicomparison method). Post-resuscitation, rats in the rhEPOVF 10-min group displayed higher mean aortic pressure associated with numerically higher cardiac index, stroke work index, and systemic vascular resistance index. rhEPO may rapidly induce myocardial protection during resuscitation from cardiac arrest.