Abstract: Objective To explore the effects of sigma-1 receptor(Sig-1R) on brain function in rats after cardiopulmonary resuscitation and its protective role in brain injury. Methods Rats were randomly assigned to four groups with 20 in each: sham-operated control (sham group), 6-hour post-resuscitation (PR 6 h group),12-hour post-resuscitation (PR 12 h group)and 24-hour post-resuscitation (PR 24 h group). In the latter three groups, cardiac arrest was induced by asphyxiation, and cardiopulmonary resuscitation was performed 6 minutes after cardiac arrest. The rats were scored for neurological deficits at 6, 12 and 24 hrs after resuscitation, respectively; after that, the rats were executed, and the expression of Sig-1R protein, mitochondrial function index, and endoplasmic reticulum stress index apoptosis index were detected by Western blot and immunohistochemistry. The correlation between Sig-1R and mitochondrial, endoplasmic reticulum stress and apoptosis indexes was evaluated. Results Compared with the sham-operated group, the rats in test group showed a gradual decrease in neurological deficit scores, Sig-1R protein expression, brain tissue adenosine triphosphate(ATP) concentration and mitochondrial membrane potential(MMP) levels at 6,12, and 24 hrs of PR(P＜0.05); CHOP protein, activated cleaved caspase-12 and cleaved caspase-3 protein expression were consistently elevated (P＜0.05). In addition, Sig-1R was negatively correlated with brain tissue endoplasmic reticulum stress and apoptosis(P＜0.05) but positively correlated with mitochondrial membrane potential level (P＜0.05). Conclusions Sig-1R expression in rat brain tissue correlates with brain injury after cardiopulmonary resuscitation and potential mechanism seems to be neuronal protection through modulating mitochondrial function and endoplasmic reticulum stress.

Key words: cardiopulmonary resuscitation after cardiac arrest, global cerebral ischemia-reperfusion injury, sigma-1 receptor, mitochondria, endoplasmic reticulum stress