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BACKGROUND: Our group previously reported that right-sided vagus nerve stimulation (RVNS) signifi cantly improved outcomes after cardiopulmonary resuscitation (CPR) in a rat model of cardiac arrest (CA). However, whether left-sided vagus nerve stimulation (LVNS) could achieve the same eff ect as RVNS in CPR outcomes remains unknown.METHODS: A rat model of CA was established using modified percutaneous epicardial electrical stimulation to induce ventricular fi brillation (VF). Rats were treated with LVNS or RVNS for 30 minutes before the induction of VF. All animals were observed closely within 72 hours after return of spontaneous circulation (ROSC), and their health and behavior were evaluated every 24 hours. RESULTS: Compared with those in the RVNS group, the hemodynamic measurements in the LVNS group decreased more notably. Vagus nerve stimulation (VNS) decreased the serum levels of tumor necrosis factor-alpha (TNF-α) and the arrhythmia score, and attenuated inflammatory infiltration in myocardial tissue after ROSC, regardless of the side of stimulation, compared with fi ndings in the CPR group. Both LVNS and RVNS ameliorated myocardial function and increased the expression of α-7 nicotinic acetylcholine receptor in the myocardium after ROSC. Moreover, a clear improvement in 72-hour survival was shown with VNS pre-treatment, with no signifi cant diff erence in effi cacy when comparing the laterality of stimulation.CONCLUSIONS: LVNS may have similar eff ects as RVNS on improving outcomes after CPR.

The present study investigated the effects of the ultrasound (US), a noninvasive technique, on ischemia-reperfusion injury (IRI) following cardiopulmonary resuscitation (CPR). The animals used in the present study were randomized into five groups (n=8 per group) as follows: i) The CPR group, where the rats underwent 6 min of untreated ventricular fibrillation (VF) followed by CPR and defibrillation; ii) the US group, in which the treatment was identical to the CPR group with the exception that rats were exposed to US treatment 24 h prior to CPR; iii) the MLA group, in which the treatment was identical to the US group with the exception that the α7 nicotinic acetylcholine receptor (α7nAChR) antagonist MLA (4 mg/kg) was administered 30 min prior to US and VF respectively; iv) the GTS group, in which the treatment was identical to the CPR group with the exception that the α7nAChR agonist GTS-21 (4 mg/kg) was injected 30 min prior to VF; and v) the SHAM group, in which the rats were exposed to surgical preparation without CPR and US application. At 1 day prior to CPR, the US treatment was administered to the left kidney by US pulses (contrast general mode with 9 MHz) with a bursting mechanical index of 0.72 for 2 min. Following treatment of the left kidney, the right kidney was exposed to identical US treatment for an additional 2 min. The results demonstrated that US preconditioning decreased the number of defibrillations required and shortened the duration of CPR. US also suppressed tumor necrosis factor-α and interleukin-6 levels following resuscitation (P<0.05), and a significantly longer overall survival time was observed in the US-treated animals (P<0.01). In addition, US attenuated neuronal injury and promoted the expression of α7nAChR in hippocampal neurons (P<0.05). However, the protective effects of US were abolished by MLA and imitated by GTS-21. The results of the present study demonstrated that prior exposure to US may improve animal outcomes following CPR, and the protective effects of US may be dependent on the cholinergic anti-inflammatory pathway (CAP) via α7nAChR.

Introduction: Recently it was shown that the ultrasound (US) treatment prevented renal ischemia- reperfusion injury (IRI) in mice. In the present study, we investigated the effects of the US treatment against IRI after CPR . Hypothesis: US would improve the outcomes after resuscitation in a rat model of CPR, and the protective effect of US would be dependent on the cholinergic anti-inflammatory pathway (CAP) via α7nAChR. Methods: The animals were randomized into 5 groups (n=8 each): (1) CPR group: the rats underwent 6 mins of untreated ventricular fibrillation (VF) followed by CPR and defibrillation; (2) US group: the treatment was identical to the CPR group except that rats were exposed to US treatment 24h before CPR; (3) MLA group: the treatment was identical to the US group except thatα7nAChR antagonist MLA (4mg/kg) was administered 30 mins prior to US treatment and VF respectively; (4) GTS group: the treatment was identical to the CPR group except that α7nAChR agonist GTS-21(4mg/kg) was injected 30 mins before VF. (5) SHAM group: the rats were exposed to surgical preparation without CPR and US application. One day before CPR, the US treatment was delivered to the left kidney by US pulses (contrast general mode with 9 MHz) with a bursting mechanical index of 0.72. US pulses were 1 second in duration and were applied once every 6 seconds for 2 mins. After the treatment of the left kidney, the right kidney was exposed to US treatment for another 2 mins. Results: Significantly longer duration of survival was observed in US-treated animals. And US treatment also suppressed the TNF-α and IL-6 following resuscitation, and improved neurological function. The expression of α7nAChR were promoted in hippocampal neurons in US group. Moreover, the protective effect of US treatment could be abolished by MLA and imitated by GTS-21. Conclusions: US treatment before IRI improves the outcomes after CPR, and CAP via α7nAChR plays an important role during CPR.