Cardioprotection via vagus nerve stimulation preconditioning: Reducing ischaemia-reperfusion injury and arrhythmic risk.

Acute myocardial infarction is a leading cause of morbidity and mortality, with ischaemia-reperfusion (I/R) injury exacerbating myocardial damage. Vagus nerve stimulation (VNS) has been reported to exert cardioprotective effects, but its efficacy in preconditioning against I/R injury requires further investigation. We evaluated the cardioprotective effects of VNS preconditioning in a rat model of acute myocardial infarction with induced I/R injury. Sixty rats were randomized into Pre-VNS, Control and Sham groups. The Pre-VNS group received 1 week of low-level cervical VNS before induction of I/R injury; stimulation was deactivated 30 min before ischaemia. Survival, echocardiographic function, reperfusion arrhythmias, arrhythmia inducibility, infarct size, apoptosis and inflammatory cytokines were assessed. Survival did not differ significantly between Pre-VNS and Control groups (75.0% vs. 65.0%, p = 0.497). However, Pre-VNS animals exhibited preserved cardiac function, with higher ejection fraction and fractional shortening (p < 0.001). VNS preconditioning reduced the incidence of reperfusion arrhythmia during left anterior descending coronary artery ligature release (p = 0.006) and decreased the arrhythmia index on programmed stimulation (p = 0.003). Infarct size and cardiomyocyte apoptosis were significantly attenuated (p < 0.001), accompanied by markedly lower serum interleukin-1β, interleukin-6 and tumour necrosis factor-alpha levels (p < 0.001). VNS preconditioning effectively mitigates I/R injury by improving cardiac function, reducing infarct size and arrhythmias, and attenuating inflammatory and apoptotic responses.