Abstract

Postoperative ileus (POI) after abdominal surgery significantly lowers the life quality of patients and increase hospital costs. However, few treatment strategies have successfully shortened the duration of POI. Electroacupuncture (EA) is a modern way of administering acupuncture and widely used in various gastrointestinal (GI) diseases in the world. Here, we studied the effect of EA on POI and its underlying mechanisms. Intestinal manipulation resulted in significant delays of GI transit, colonic transit and gastric emptying. Surgery also up-regulated c-fos in nucleus of the solitary tract (NTS) and induced inflammation response in the small intestine. Further, operation and inhale anesthesia inhibited NTS neuron excitation duration for the whole observation time. EA administered at ST36 indeed shortened the recovery time of GI and colonic transit, and significantly increased the gastric emptying. EA also significantly activated the NTS neurons after operation. However, there was no anti-inflammation effect of EA during the whole experiment. Finally, atropine blocked the regulatory effect of EA on GI function, when it was injected after surgery, but not before surgery. Thus, the regulatory effect of EA on POI was mainly mediated by exciting NTS neurons to improve the GI tract transit function but not by activating cholinergic anti-inflammatory pathway.

Highlights

  • Postoperative ileus (POI) after abdominal surgery significantly lowers the life quality of patients and increase hospital costs

  • The fluorescent marker remaining in the stomach of the EA group was less than that of the model and sham EA groups, with a distributed to sb-6 (Fig. 1E)

  • The above data indicate that intestinal manipulation (IM) caused a clinically relevant POI and EA treatment partly mitigated the delay of GI transit up to 24 h after surgery

Read more

Summary

Introduction

Postoperative ileus (POI) after abdominal surgery significantly lowers the life quality of patients and increase hospital costs. The regulatory effect of EA on POI was mainly mediated by exciting NTS neurons to improve the GI tract transit function but not by activating cholinergic anti-inflammatory pathway. Secretion of cytokines (IL-6, TNF-α) from monocytes and smooth muscle inhibitory substances (NO, COX-2) contribute to the delay in intestinal transit[7,8] These events delay GI transit, decrease local neuromuscular function and inhibit neurogenic pathways, thereby suppressing motility along the entire gastrointestinal tract for sustained postoperative periods[9,10]. Electrical stimulation of the vagus efferent nerve or drug stimulation of the nucleus of the solitary tract (NTS), the parasympathetic preganglionic center, reduces the inflammatory response and POI via the cholinergic anti-inflammatory pathway[14,15]. EA promotes the GI function and some reports have shown therapeutic www.nature.com/scientificreports/

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call