Published online Mar 28, 2022. doi: 10.3748/wjg.v28.i12.1239
Peer-review started: September 21, 2021
First decision: November 7, 2021
Revised: November 22, 2021
Accepted: February 16, 2022
Article in press: February 16, 2022
Published online: March 28, 2022
Processing time: 184 Days and 21 Hours
Neuraxial anesthesia has been shown to exert a positive effect on intestinal microvascular perfusion. In an animal model of sepsis, thoracic epidural anesthesia was demonstrated to ameliorate perfusion deficits in the muscularis and mucosal layers of the gut. However, whether spinal aneathesia as a neuraxial anesthesia affects intestinal inflammation in inflammatory bowel disease (IBD) is still unclear.
The exact etiology of IBD remains unknown, and the imbalance of the gut microbiota is related to the occurrence and progression of IBD. The bidirectional between the brain and gut microbiota has gradually attracted more attention. Finding interventions on the brain-gut axis will be a new vision.
A dextran sodium sulfate (DSS)-induced colitis mouse model was established to explore the role of spinal anesthesia in IBD and to identify the potential mechanisms involved.
A DSS-induced colitis mice model was established, and then we used spinal anesthesia on colitis mice to explore the role of spinal anesthesia in IBD and identify the potential mechanisms involved. Moreover, cohousing and fecal microbiota transplantation were used to help mice from separate lines share microbes across cocaged individuals.
This study clearly revealed that spinal anesthesia inhibited the development of DSS-induced colitis in mice. We demonstrated that spinal anesthesia alleviated intestinal inflammation, maintained immunological function, and improved intestinal barrier function by modulating the gut microbiota. Reducing the increase in noradrenaline levels in DSS-treated mice by spinal anesthesia could be one of the mechanisms underlying the effect on the gut microbiota.
The study implied a positive effect of spinal anesthesia in relieving intestinal inflammation, protecting intestinal barrier function, and regulating the intestinal microflora in an IBD mouse model. Decreasing the noradrenaline level would be a possible mechanism of spinal anesthesia.
The present study provided evidence supporting the protective effects of spinal anesthesia on IBD by modulating gut microbiota, which highlights a novel approach for the treatment of IBD.