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Studies have demonstrated that Win55,212-2 induced pharmacological hypothermia and protected the neurological function after cardiopulmonary resuscitation (CPR) in a rat cardiac arrest (CA) model. However, the mechanism is still unclear. In this study, we investigated if c-fos was also involved in this mechanism.
CA was induced by transesophageal ventricular pacing in SD rats. 5min after onset of CA, CPR was started. After 30 min of ROSC, 30 animals were randomized into either Win55, 212-2 group (animals in drug groups were received continuous intravenous infusion of Win55,212-2 with 1 mg/kg/h for 4 h) or Normothermic group (animals were received 5% DMSO). Rats in normothermic group were maintained at 37°C with warming lamp though the whole experiment. Rats in drug group were warmed to 37°C increasingly after 4h of Win55,212-2 treatment. Brains of five animals in each group were harvested for detecting c-fos by RT-PCT and Western blot at 24 h after ROSC respectively.
Temperatures of animals in Win55,212-2 group decreased to 34°C in 4 hours after ROSC, and the survival of which were longer than that of the control group. The expression of c-fos was significantly higher in the Win55, 212-2 group than that of control group.
c-fos participated the neouprotection of Win 55,212-2 after CPR in a rat CA model.