Abstract 2629: High Dose Erythropoietin Improves the Postresuscitation Myocardial Dysfunction and Survival in an Appropriate Therapeutic Time Window
Introduction: The myocardial dysfunction carries high mortality rate in the postresuscitation period. Interventions for improving myocardial dysfunction may improve the outcomes of resuscitated victims. The erythropoietin (EPO) provides protective effects for the myocardium with ischemia-reperfusion injuries. However, its effects on the treatment of cardiopulmonary arrest and post-resuscitation myocardial dysfunction remain unknown.
Hypothesis: EPO can improve the postresuscitation myocardial dysfunction in an appropriate therapeutic time window.
Methods: Asphyxia-induced cardiac arrest was performed in male adult Wistar rats. Cardiopulmonary resuscitation including chest compressions, mechanical ventilation and epinephrine (0.01 mg/kg) was begun after 6.5 or 9.5 minutes of asphyxia. Animals were randomized to undergo treatment with intravenous EPO (5000 U/kg) or equivalent volume of 0.9% saline placebo. These agents were administrated 3 minutes after the return of spontaneous circulation.
Results: The better left ventricular dP/dt40 (2958±827 vs. 1321±1200 mmHg/s, P<0.05) and maximal -dP/dt (2562±546 vs. 745±877 mmHg/s, P<0.05) at 120 minutes after cardiac arrest, and better left ventricular fraction shortening (32.0 ± 2.0 vs. 24 ± 6.7 %, P<0.05) by echocardiography at 90 minutes after cardiac arrest were noted in the EPO-treated group compared to the control group in the condition of 6.5 minutes of asphyxia. The EPO treated group had better neurological recovery at 24 hours after resuscitation. Survival rate at 72 hours after 6.5 minutes of asphyxia was better in the EPO-treated group (50% vs. 20 %, P=0.02). No animal survived 72 hours after 9.5 minutes of asphyxia either in EPO-treated or control group. More activation of cardiac Akt and ERK 42/44 signaling pathways were noted in the EPO-treated group than the control group.
Conclusions: EPO has the potential to improve postresuscitation myocardial dysfunction and short term survival in rats after asphyxia-induced cardiac arrest in an appropriate therapeutic time window.