Selenium as a potential treatment in cardiac arrest induced global cerebral ischemia

Abstract

Survival from out-of-hospital cardiac arrest has not significantly improved during the last decades, despite tremendous efforts in research. Nevertheless, the observation that additional neuronal damage may occur after initial successful resuscitation ensuing reperfusion of the brain gives an extended window of opportunity to modify neurological outcome by therapeutic measures. To date, the only clinically effective tool for amelioration of brain injury after cardiac arrest is immediate mild hypothermia, whereas the results of pharmacological approaches have been largely disappointing. Consequently, the search for additional therapeutic options is still ongoing including strategies to counteract the deleterious effects of oxygen-derived free radicals following cerebral reperfusion. The trace element selenium forms an essential component of the enzyme glutathione peroxidase and other seleno-organic compounds which are part of the endogenous defense against oxidative injury. According to a recently published retrospective study, early administration of intravenous selenium was a significant predictor of regaining consciousness after cardiac arrest, whereas overall survival at 6 months follow-up was not influenced significantly. These results lead to the hypothesis that early administration of selenium may improve neurological outcome after cardiopulmonary resuscitation. Future prospective randomized studies are needed to validate this assumption, preferably testing selenium as add-on therapy in patients undergoing therapeutic hypothermia after cardiac arrest.