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The aim of the study was to establish a ventricular fibrillation (VF) cardiac arrest (CA) resuscitation model with consistent neurologic and neuropathologic damage as potential therapeutic target.Prospectively randomized groups of experiments in two phases. In phase 1 four groups of male Sprague–Dawley rats (n = 5) were resuscitated after 6 min VFCA with 2 and 6 min basic life support durations (BLS) with and without adrenaline. In phase 2 the most promising group regarding return of spontaneous circulation (ROSC) and survival was compared with a group of 8 min CA. Resuscitability, neurologic deficit scores (NDS), and overall performance category (OPC) were assessed daily; histolopathology of the hippocampal CA1 region [hematoxylin and eosin- (viable neurons), Fluoro-Jade- (dying neurons), and Iba-1 immunostaining (microglial activation–semiquantitative)] on day 14.Two minutes BLS and with adrenaline as most promising group of phase 1 compared with an 8 min group in phase 2 exhibited ROSC in 8 (80%) vs. 9 (82%) animals and survivors till day 14 in 7 (88%) (all OPC 1, NDS 0 ± 0) vs. 6 (67%) (5 OPC 1, 1 OPC 2, NDS 0.83 ± 2.4) animals. OPC and NDS were only significantly different at day 1 (OPC: P = 0.035; NDS: P = 0.003). Histopathologic results between groups were not significantly different; however, a smaller variance of extent of lesions was found in the 8 min group. Both CA durations caused graded neurologic, overall, such as histopathologic damage.This dynamic global ischemia model offers the possibility to evaluate further cognitive and novel neuroprotective therapy testing after CA.