| Background:Sphincter of Oddi (SO) is a circular shape smooth muscle in joint position of distal end of common bile duct and duodenum. Sphincter of Oddi dysfunction (SOD) which may leads to abnormal flow of bile and pancreatic juice play an important role in pathophysiology of many biliary and pancreatic diseases. Reinforcement of SO tone by biliary calculus or biliary sludge, CCK and Alcohol may cause obstruction of distal biliary tract and pancreatemphraxis, which lead to reflux of bile and pancreatic juice, and is one of the major causes of acute pancreatitis. While reinforcement of SO tone also has a close relationship with tissues around the sphincter. SO manometry (SOM) to patients with pancreatitis found the fact that SO tone was raised. But up to now, we have not made clear whether this change is etiological factor or sequence of pancreatitis.Endothelin, a novel vasoconstrictor peptide produced by vascular endothelial cells, may also mediate contraction in non-vascular muscles. Vascular endothelial cells and acinar cells of pancreas are found to produce. ET. The elevated ET-1 plasma levels during pancreatitis may induce systemic sequence and other organ dysfunction. SO also belongs to smooth muscles and its function proberbly affected by ET-1. Aims:To determine whether SOD is not only one of the causes but also apathophysiological change of severe acute pancreatitis by studying the relationship between the motility of SO and ET-1 plasma levels in experimental models of severe acute pancreatitis in rabbits. We also attempt to make clear the role of SOD in pathophysiological process of severe acute pancreatitis and its mechanisms. Methods:Experimental models of severe acute pancreatitis in rabbits were developed to study the dynamic changes of SO motility by SOM. Meanwhile radio-immunity analysis (RIA) was used to detect the dynamic changes of ET-1 plasma levels. These two changes were compared by statistical analysis.Eleven rabbits of either sexes, weighting 3.8-4.8 kg, were used and random assorted to two groups, they were fasted in the morning of surgery but had free access to water. They were then anesthetized with Ig/kg urethane intravenously. A steel catether was inserted into the right carotid artery to allow blood sampling.Fixing the front-end sac of condom and B-D segmental eqidural catheter together through double ligation of silk suture made fluid sac for manometry. The sac was filled with saline and air bubble should be eliminated. Then saline inside the sac should be drew out by syringe connected to the distal end of the catheter to make the sac retraction and attached to the catheter.After an upper median laparotomy, the biliary tree was identified. An open tipped catheter (OD 1 .0mm) was proximally placed and used to siphon off the hepatic bile. The fluid sac for manometry (OD 1.7mm) was distally inserted into the choledochoduodenal junction, and then withdrawn 1mm and tied in the bile duct to avoid any leaks or occlusion of the catheter. The pressure changes were recorded on amultichannel polygraphic recorder through an external pressure transducer, which was connected to a triplet divider that also connected to the manometry catheter and the syringe. The sac was filled with 0.05ml saline in vitro and the pressure of this time was set as zero reference. When manometry, the sac insides SO was refilled with 0.05ml saline to the extent of no shape or color changes of SO were finding. Closed the syringe tip of the triplet divider to let SO pressure transmitted to the pressure transducer through the manometry catheter. All preparations were allowed to stabilize for 30 minutes prior to SOM. Pressure recording reflect changes in the resistance of the sphincter to flow, tonic activity, superimposed phasic wave contractions and frequency of phasic contraction were recorded by the pressure changes induced by muscular activity.After recording normal SO pressure for 30 minutes, seven rabbits were injected with 5% sodium tauroglycocholate (NaTC) in six fixed points isodis...
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