Electroacupuncture treatment partly promotes the recovery time of postoperative ileus by activating the vagus nerve but not regulating local inflammation

Postoperative ileus (POI) is a common complication after abdominal surgeries that causes temporary bowel paralysis, resulting in nausea, vomiting, abdominal distension, and prolonged hospital stay. This condition significantly increases hospital costs and reduces patient quality of life. Although several therapeutic strategies have been proposed over the past decade, few have demonstrated real efficacy in reducing the duration of POI. Electroacupuncture (EA), a modern modality that combines traditional acupuncture with electrical stimulation, has shown promising results in the treatment of gastrointestinal disorders, but its specific mechanisms in POI remained poorly understood.

This experimental study used 192 rats divided into four groups to systematically investigate the effects of EA on POI and its underlying mechanisms. The POI model was induced through standardized intestinal manipulation during laparotomy, simulating real clinical conditions. EA was applied at the Zusanli point (ST-36) bilaterally, at a frequency of 5 Hz and intensity of 1–2 mA, throughout the perioperative period. Results demonstrated that intestinal manipulation produced significant delays in gastrointestinal transit, colonic transit, and gastric emptying, accompanied by an intense local inflammatory response.

Surgery also induced important neurophysiologic changes, including increased c-fos expression in the nucleus of the solitary tract (NTS) and prolonged inhibition of neuronal excitation in this region. EA proved effective in accelerating recovery of gastrointestinal function, especially 24 hours after the surgical procedure. Treatment significantly improved gastrointestinal transit (geometric center increased from 2.49 to 3.54), reduced colonic transit time, and increased gastric emptying compared with the model group. Crucially, EA also significantly restored excitation of NTS neurons after surgery, suggesting activation of the vagal nervous system.

However, contrary to expectations based on the cholinergic anti-inflammatory pathway, EA did not show any anti-inflammatory effect throughout the experiment. There was no reduction in leukocyte infiltration in the intestinal wall or in the expression of pro-inflammatory cytokines (IL-1β and TNF-α). To confirm the role of the vagus nerve, the investigators used atropine, a cholinergic antagonist, at different time points. When administered before surgery, atropine did not affect the benefits of EA, but when given after surgery it completely blocked the therapeutic effects of EA on gastrointestinal transit.

These findings indicate that the therapeutic effect of EA on POI is mediated mainly through excitation of NTS neurons to improve gastrointestinal transit function, not through the cholinergic anti-inflammatory pathway. The clinical implications of this study are significant, as they provide robust scientific evidence for the use of EA as adjuvant therapy in the management of POI. The treatment proved safe and effective, offering a non-pharmacologic alternative for accelerating postoperative recovery. Limitations include the animal model, which may not fully reflect the complexity of human POI, and the absence of anti-inflammatory effects, which requires further investigation of optimized EA protocols.