Objective：To investigate the effect of electrical stimulation to sacral spinal nerve 3 （S3 stimulation） on gastrointestinal dysfunction after spinal cord injury （SCI）.Methods：Six rabbits were taken as normal controls to record their gastrointestinal multipoint biological discharge,colon pressure and rectoanal inhibitory reflex.Electrodes were implanted into S3 in another 18 rabbits.Then the model of SCI was conducted following Fehling＇s method：the rabbit S3 was clamped to induce transverse injury,which was claimed by both somatosensory evoked potential and motion evoked potential.Two hours after SCI,S3 stimulation was conducted.The 18 rabbits were subdivided into 3 groups to respectively record their gastrointestinal electric activities （n=6）,colon pressure （n=6）,and rectum pressure （n=6）.Firstly the wave frequency was fixed at 15 Hz and pulse width at 400 μs and three stimulus intensities （6 V,8 V,10 V） were tested.Then the voltage was fixed at 6 V and the pulse width changed from 200 μs,400 μs to 600 μs.The response was recorded and analyzed.The condition of defecation was also investigated.Results：After SCI,the mainly demonstrated change was dyskinesia of the single haustrum and distal colon.The rectoanal inhibitory reflex almost disappeared.S3 stimulation partly recovered the intestinal movement after denervation,promoting defecation.The proper stimulus parameters were 15 Hz,400 μs,6 V,10 s with 20 s intervals and 10 min with 10 min intervals,total 2 h.Conclusion：S3 stimulation is able to restore the intestinal movement after denervation （especially single haustrum and distal colon）,which promotes defecation.
Objective: To observe the ultrastructural change of the route of gut bacterial translocation in a rat with spinal cord injury(SCI).Methods: Forty Wistar rats were divided into the following groups: control group and 3 SCI groups(10 in each group). The rats in the SCI groups were established SCI model at 24 h, 48 h, and 72 h after SCI. Small intestine mucous membrane tissue was identified and assayed by transmission electron microscope, scanning electron microscope and immunofluorescence microscopy. Results: Small intestine mucous membrane tissue in control group was not damaged significantly, but those in SCI groups were damaged significantly. Proliferation bacteria in gut lumen attached on microvilli. The extracellular bacteria torn the intestinal barrier and perforated into the small intestinal mucosal epithelial cell. The bacteria and a lot of particles of the seriously damaged region penetrated into the lymphatic system and the blood system directly. Some bacteria were internalized into the goblet cell through the apical granule. Some bacteria and particles perforated into the submucosa of the M cell running the long axis of M cells through the tight junctions. In the microcirculation of mucosa, the bacteria that had already broken through the microvilli into blood circulation swim accompanying with erythrocytes. Conclusion: The routes of bacterial translocation interact and format a vicious circle. At early step, the transcellular pathway of bacterial translocation is major. Following with the destroyed small intestine mucous, the routes of bacterial translocation through the lymphatic system and the blood system become direct pathways. The goblet cell-dendritic cell and M cell pathway also play an important role in the bacterial translocation.
