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Introduction: Cardiac arrest significantly increases endogenous catecholamines, which worsens myocardial dysfunction and increases whole body oxygen consumption after resumption of spontaneous circulation (ROSC). In animal studies, blockade of adrenergic effects caused by elevated catecholamines immediately after cardiopulmonary resuscitation (CPR) showed improvement in post arrest cardiac function. Dexmedetomodine has shown sympatholytic effects in previous studies and may improve myocardial function after ROSC. Hypothesis: Dexmedetomidine given during CPR decreases the sympathetic response thereby improving stroke volume (SV) and cardiac output (CO) after ROSC compared with standard CPR. Methods: Sixteen anesthetized & ventilated (2 months old) farm pigs of either sex were blindly randomized (8/group) after induction of VF to receive either Dex (2 mcg/kg) or placebo after the first minute of chest compressions. Chest compressions were delivered at 100/min by a pneumatic compressor device (Thumper) and 21% FiO2 was used for ventilation. Epinephrine levels were measured at baseline, before the onset of CPR, at the time of ROSC and two hours after ROSC. SV and CO were measured at 15, 30, 60, 90 and 120 minutes after ROSC using a Pressure-Volume catheter in the left ventricle. We used generalized estimating equations (SAS Proc Genmod) to determine the relationship among log %baseline Epinephrine, time and drug group. Results: There were 6 surviving animals in the placebo group and 8 in the Dex group. The duration of CPR was not significantly different in the two groups (p=0.2273). Across all time points, the Dex group had on average log (%baseline Epinephrine) that was 1.68 lower than the log (%baseline) for the saline group (p=0.0252). The Dex group had significantly less decrease in SV from baseline (69.6 ± 30.8; vs. 52.8 ± 21.5; p=0.0002). SV was significantly lower at 15 min (p=0.0034) and 30 min (p=0.055) with only a trend towards lower values after that. The Dex group had significantly less decrease in CO from baseline (80.3 ± 45.1; vs. 49.6 ± 17.3; p=0.0001). CO was significantly lower at 15 min (p=0.0056) and 30 minutes (p=0.0282) with only a trend towards lower values after that. Conclusions: Dex, when given during the initial cycle of chest compressions during CPR, decreases the sympathetic response thereby increasing the SV and CO early post ROSC. Further studies are needed to evaluate the appropriate dose, continuous infusion and time of administration.