Abstract

Introduction: Studies have demonstrated that vagus nerve stimulation (VNS) reduces ischemia reperfusion (I/R) injury. In this study, we investigated the protective effects of VNS in a rat model of cardiopulmonary resuscitation (CPR). We further investigated whether the beneficial effects of VNS were dependent on the alpha 7 nicotinic acetylcholine receptor (α7nAChR). Methods: The animals were randomized into 4 groups (n=10 each): (1) CPR group (n=10): the rats underwent 8 mins of untreated ventricular fibrillation (VF) followed by 8 mins of CPR and defibrillation. The right vagus nerve was exteriorized but not stimulated.; (2) VNS group (n=10): the treatment was identical to the CPR group except that VNS was initiated at the beginning of precordial compression and continued for 4 hours after the return of spontaneous circulation(ROSC); (3) MLA group(n=10): the treatment was identical to the VNS group except that α7nAChR antagonist MLA (5mg/kg) was administered intraperitoneally (IP) 15 mins prior to VF; (4) GTS group(n=10): the treatment was identical to the CPR group except that α7nAChR agonist GTS-21 (5mg/kg) was IP injected 30 mins before VF. Blood gases, post resuscitation myocardial and cerebral function and the duration of survival were monitored in all animals. Results: There were no differences in mean arterial pressure among 4 groups. Significantly better post-resuscitation myocardial and cerebral functions and longer durations of survival were observed in VNS-treated animals, and these protective effects of VNS could be abolished by MLA and imitated by GTS-21 indicating that these beneficial effects might be dependent on a7nAChR (Figure *P<0.05 vs CPR, **P<0.01 vs CPR, ##P<0.01 vs MLA). In addition, VNS decreased the number of electric shocks and the length of CPR duration. Conclusion: VNS improves the outcomes after CPR and cholinergic anti-inflammatory pathway via α7nAChR plays an important role during CPR.

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