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BackgroundThere is growing evidence about the effect of bilateral superior cervical sympathectomy on myocardial ischemia-reperfusion (I/R) injury. Studies have increasingly found that the signal transducer and activator of transcription 3 (STAT3) plays a protective role in myocardial I/R injury. However, the precise mechanism is unknown. The present study explored the bilateral superior cervical sympathectomy’s effect and potential mechanism in mice myocardial I/R injury.MethodsThe left heart I/R injury model was created by ligating the anterior descending branch of the coronary artery for 30 min followed by reperfusion. Bilateral superior cervical sympathectomy was performed before myocardial I/R injury. To evaluate the effect of bilateral superior cervical sympathectomy on the myocardium, we examined the myocardial infarct size and cardiac function. Then, myocardial apoptosis, inflammation, and oxidative stress were detected on the myocardium. Furthermore, the expression of STAT3 signal in myocardial tissue was measured by western blotting. To further examine the cardioprotective effect of STAT3 after bilateral superior cervical sympathectomy, the STAT3 inhibitor (static) was utilized to inhibit the phosphorylation of STAT3.ResultsThe results showed that the myocardial I/R injury decreased and the cardiac function recovered in the myocardial I/R injury after cervical sympathectomy. Meanwhile, cervical sympathectomy reduced the myocardial distribution of the sympathetic marker tyrosine hydroxylase (TH) and systemic sympathetic tone. And levels of oxidative stress, inflammatory markers, and apoptosis were reduced in myocardial tissue. We also found that the STAT3 signal was activated in myocardial tissue after cervical sympathectomy. STAT3 inhibitor can partially reverse the myocardial protective effect of cervical sympathectomy.ConclusionBilateral superior cervical sympathectomy significantly alleviated myocardial I/R injury in mice. And activation of the STAT3 signal may play an essential role in this.