| People | Locations | Statistics |
|---|---|---|
| Naji, M. |
| |
| Motta, Antonella |
| |
| Aletan, Dirar |
| |
| Mohamed, Tarek |
| |
| Ertürk, Emre |
| |
| Taccardi, Nicola |
| |
| Kononenko, Denys |
| |
| Petrov, R. H. | Madrid |
|
| Alshaaer, Mazen | Brussels |
|
| Bih, L. |
| |
| Casati, R. |
| |
| Muller, Hermance |
| |
| Kočí, Jan | Prague |
|
| Šuljagić, Marija |
| |
| Kalteremidou, Kalliopi-Artemi | Brussels |
|
| Azam, Siraj |
| |
| Ospanova, Alyiya |
| |
| Blanpain, Bart |
| |
| Ali, M. A. |
| |
| Popa, V. |
| |
| Rančić, M. |
| |
| Ollier, Nadège |
| |
| Azevedo, Nuno Monteiro |
| |
| Landes, Michael |
| |
| Rignanese, Gian-Marco |
|
Weihs, Wolfgang
in Cooperation with on an Cooperation-Score of 37%
Topics
Publications (1/1 displayed)
Places of action
| Organizations | Location | People |
|---|
article
Establishing a Rodent Model of Ventricular Fibrillation Cardiac Arrest With Graded Histologic and Neurologic Damage With Different Cardiac Arrest Durations
Abstract
<jats:title>ABSTRACT</jats:title><jats:sec><jats:title>Purpose:</jats:title><jats:p>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.</jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p>Prospectively randomized groups of experiments in two phases. In <jats:italic toggle="yes">phase 1</jats:italic> 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 <jats:italic toggle="yes">phase 2</jats:italic> 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.</jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p>Two minutes BLS and with adrenaline as most promising group of <jats:italic toggle="yes">phase 1</jats:italic> compared with an 8 min group in <jats:italic toggle="yes">phase 2</jats:italic> 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: <jats:italic toggle="yes">P</jats:italic> = 0.035; NDS: <jats:italic toggle="yes">P</jats:italic> = 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.</jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p>This dynamic global ischemia model offers the possibility to evaluate further cognitive and novel neuroprotective therapy testing after CA.</jats:p></jats:sec>