Systemic inflammation is a potentially debilitating complication of thoracic surgeries with significant physical and economic morbidity. There is compelling evidence for the role of the central nervous system in regulating inflammatory processes through humoral mechanisms. Activation of the afferent vagus nerve by cytokines triggers anti-inflammatory responses. Peripheral electrical stimulation of the vagus nerve in vivo during lethal endotoxemia in rats inhibited tumor necrosis factor synthesis and prevented shock development. However, the vagal regulatory role of systemic inflammation after lung lobectomy is unknown.

One hundred patients who underwent lobectomy via thoracotomy were recruited and equally randomized to treated group or controls. Intermittent stimulation of the auricular branch of vagus nerve in the triangular fossa was applied in the treated group using neurostimulator V (Ducest^®, Germany), starting 24 h preoperatively and continued till the 4th postoperative day (POD). Inflammatory interleukins (IL) were analyzed using ELISA preoperatively, on the 1st and 4th POD.

On the 1st POD, patients who underwent neurostimulation had reduced serum concentrations of CRP (p = 0.01), IL6 (p = 0.02) but elevated IL10 (p = 0.03) versus controls. On the 4th POD, serum concentrations of CRP, IL6 and IL10 were similar in both groups. Moreover, the treated group was associated with lower incidence of pneumonia (p = 0.04) and shorter hospitalization time (p = 0.04) versus controls.

Modulations in the brain stem caused by noninvasive transcutaneous stimulation of the vagus nerve after lung lobectomy attenuate the acute postsurgical inflammatory response by the regulation of IL6 and IL10, resulting in  reduced incidence of postoperative pneumonia and short hospitalization time.

NCT03204968.