Establishing a Rodent Model of Ventricular Fibrillation Cardiac Arrest with Graded Histologic and Neurologic Damage with Different Cardiac Arrest Durations

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Abstract

Purpose:

To establish a ventricular fibrillation (VF) cardiac arrest (CA) resuscitation model with consistent neurologic and neuropathologic damage as potential therapeutic target.

Methods:

Prospectively randomized groups of experiments in 2 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 to 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 Immuno-staining (microglial activation – semiquantitative)] on day 14.

Results:

Two minutes BLS and with adrenaline as most promising group of phase 1 compared to 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.

Conclusions:

This dynamic global ischemia model offers the possibility to evaluate further cognitive and novel neuroprotective therapy testing after CA.

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