Objective: Overproduction of free radicals is a main factor contributing to cerebral injury after cardiac arrest (CA)/cardiopulmonary resuscitation (CPR). We sought to evaluate the impact of edaravone on the survival and neurological outcomes after CA/CPR in rats.
Methods: Rats were subjected to CA following CPR. For survival study, the rats with restoration of spontaneous circulation (ROSC) were randomly allocated to one of the two groups (edaravone and saline group, n=20/each group) to received Edaravone (3 mg/kg) or normal saline. Another 10 rats without experiencing CA and CPR served as the sham group. Survival was observed for 72 hours and the neurological deficit score (NDS) was calculated at 12, 24, 48, and 72 hours after ROSC. For the neurological biochemical analysis study, rats were subjected to the same experimental procedures. Then, edaravone group (n=24), saline group (n=24) and sham group (n=16) were further divided into 4 subgroups according to the different time intervals (12, 24, 48, and 72 hours following ROSC). Brain tissues were harvested at relative time intervals for evaluation of oxidative stress, TUNEL staining and apoptotic gene expression.
Results: Edaravone improved postresuscitative survival time and neurological deficit, decreased brain malonylaldehyde level, increased superoxide dismutase activities, decreased proapoptotic gene expression of capase-8, capase-3, and Bax, and increased antiapoptotic Bcl-2 expression at 12, 24, 48, and 72 hours after ROSC.
Conclusions: Edaravone improves survival and neurological outcomes following CPR via antioxidative and antiapoptotic effects in rats.
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