Published online Dec 15, 2003. doi: 10.3748/wjg.v9.i12.2849
Revised: May 24, 2003
Accepted: June 2, 2003
Published online: December 15, 2003
AIM: Several neural and hormonal factors are known to affect motility of sphincter of Oddi (SO). The major roles of SO are to regulate the flow of bile and pancreatic juice into the duodenum and to prevent the reflux of duodenal contents into the biliary and pancreatic duct. After pancreas transplantation, graft SO was denervated and graft pancreatitis might have relations to SO motility. The motility of SO after canine pancreas transplantation with bladder drainage was investigated.
METHODS: Normal canine SO manometry and pancreas graft SO manometry after pancreas transplantation with bladder drainage were performed in seven dogs respectively before and after cholecystokinin (CCK) administration. Data of SO basal pressure, contraction frequency, amplitude and motility index after transplantation and CCK administration were compared with that in controls and before CCK administration.
RESULTS: SO showed regular contractions with a certain basal pressure in control dogs. After transplantation, the graft SO basal pressure and contraction frequency were higher than that in controls, but the amplitude decreased (P < 0.01). There was no great difference in SO motility index. CCK administration could relax normal SO but stimulate graft SO after pancreas transplantation with bladder drainage. After CCK administration, SO basal pressure, frequency and motility index were increased significantly (P < 0.05), in comparison with that before administration. The amplitude remained unchanged (P > 0.05), in comparison with that before CCK administration.
CONCLUSION: After auto-pancreas transplantation with bladder drainage, canine SO motility was inhibited. Basal pressure and frequency increased but amplitude decreased. CCK administration after transplantation had an inhibitory effect on canine SO instead of a relaxation effect observed in normal canine SO. This will increase the resistance of SO to the pancreatic juice flow and induce pancreatic juice stagnation and can not prevent reflux of urine and duodenal contents when the bladder pressure is increased to a certain extent, which may cause graft pancreatitis.