• U Ebmeyer, G Keilhoff, G Wolf, and W Röse.
• Institute of Medical Neurobiology, Otto-von-Guericke University Magdeburg, Leipziger Strasse 44, 39120 Magdeburg, Germany. uwe.ebmeyer@medizin.uni-magdeburg.de
• Resuscitation. 2002 May 1; 53 (2): 189-200.

AbstractAn asphyxial cardiac arrest rat model, originally developed for Sprague-Dawley rats, was transferred to a Wistar rat model. Several strain specific life support adjustments, i.e. ventilator settings, anaesthesia, and drug requirements, were necessary to stabilize the model for Wistar rats. Despite these arrangements numerous resuscitation related variables appeared different. Three groups were evaluated and compared: a temperature monitored Wistar group 1 (n=34), a temperature controlled Wistar group 2 (n=26) and a temperature controlled Sprague-Dawley group 3 (n=7). Overall, Wistar rats seem to have more sensitive cardio-circulatory system evidenced by a more rapid development of cardiac arrest (164 vs. 201 s), requiring higher adrenaline/epinephrine doses (10 vs. 5 microg/kg) and requiring more time for recovery after resuscitation (i.e. for return of blood pressure and blood gases). Without strict temperature control (as in groups 2+3 rats) group 1 rats went into spontaneous mild to moderate hypothermia during the first 24 h after restoration of spontaneous circulation (ROSC). Spontaneous hypothermia delayed the development of overall visible CA1 neuronal damage 24-48 h, but did not prevent it; therefore the model seemed to be suitable for future studies. Neuronal damages in the CA1 region in Wistar rats appeared to be more as shrunken cell bodies and pyknotic nuclei before resorption took place, whereas in Sprague-Dawley rats appeared in the same region.

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