Experimental Study For Influence Of Hypercholesteremia And Cholecystectomy On The Function Of Sphincter Of Oddi

Clinically,most patients with cholecystolithiasis have no overt symptoms.The therapeutics is conventional cholecystectomy or laparoscopic cholecystectomy,which can relieve the symptoms and achieve clinic healing.After the cholecystectomy,some patients will suffer from Postcholecystectomy syndrome(PCS).Recent study shows the syndrome have no relationship with surgery itself,but with Sphincter of Oddi(SO) dyskinesia.This PCS in narrow definition is called as postcholecystectomy biliary dyskinesia.Among these patients,most of them have no structural changes,it is supposed that Sphincter of Oddi dysfunction is the main cause of the symptoms.Cholecystolithiasis is more popular in the worldwide nowadays.The essential condition of cholesterol calculus is cholesterol bile oversaturation,nucleation defect,and evacuation function of gallbladder lesion.Cholesterol bile oversaturation is the basis of cholesterol calculus.The experiment shows that after ingested hyper-cholesterol diet,the level of cholesterol in bile increase,which can induce formation of cholesterol calculus. Meanwhile,the bile containing cholesterol crystal influence the pressure of common bile duct,which can impact the function of SO.SO is a complex,valve-like,neuromuscular structure located at the junction of the bile and pancreatic ducts with the duodenum.Several neural and hormonal factors are known to mediate SO motility.The main functions of the 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-pancreatic systems.Resent reports also shown that biliary pressure directly influence the SO motility,and the mechanism might be the reflexes between SO and the gall bladder or bile duct,which is important in the regulation of SO motility.Report shows that nitric oxide(NO) is the main inhibitory transmitter released by non-adrenergic,non-cholinergic(NANC) neurons.The disposition of nitric oxide synthetase (NOS) neurons is widespread in each layers.And the amount of NOS in circular muscle layer of SO is the most abundant.To inhibit the synthesis of NO,the motility function of SO will enhance.In contrast,giving NO donor like glyceryltrinitrate locally or systematically will induce the relaxation of SO via NO oxidative product. Hypercholesteremia can influence the release or function of NO in vessel,so we suppose that hypercholesteremia can disturb the relaxation of SO too.The motility change of SO and the mechanisms of SOD during the process of hypercholesteremia and cholecystectomy have not been completely understood.The aim of this study was to explore the influence of hypercholesteremia and cholecystectomy on the motility function of SO.Furthermore,we discussed the role of NO in the mediation of SO motility.The studies were as follows:To explore the motility change of SO after cholecystectomy:A total of 16 rabbits were randomized into 2 groups.In the control group,the rabbits underwent false operation.In the experimental groups,the animals underwent cholecystectomy.After 4 weeks,all animals were examined with manometry and myoelectric activity determination of SO.In the experimental group,the pressure of common bile duct was lower,while the basal pressure of SO and the amplitude of contraction was significantly higher compared with control group.At the aspect of myoelectric activity,its state changed from spike potentials into myoelectronic activity.The amplitude was higher while the lasted time was prolonged.To investigate the effects of hypercholesteremia on motor function of sphincter of Oddi,the animals were randomized into 4 groups.In the control group,the rabbits were fed with normal diet.In the experimental groups,the animals were fed with normal diet+ cholesterol(1.2%) for 4,6,10weeks.All animals were examined with manometry and myoelectric activity determination of SO.In the experimental group,the pressure of common bile duct was lower,while the basal pressure of SO and the amplitude of contraction was significantly higher compared with control group.In myoelectric activity, its state changed from spike potentials into myoelectronic activity.The amplitude was higher while the lasted time was prolonged.The frequency has no overt change.The animals fed with normal diet+cholesterol(1.2%) for 6 weeks were under cholecystectomy. After 4 weeks,we found that the lesions on the function of SO lasted and aggravated. Cholecystectomy enhances the degree of impair. After animal experiments,we obtained some SO samples to detect NO content.Result showed that the content change of NO was not obvious in cholecystectomy group. Meanwhile,in hypercholesteremia groups,the content of NO depressed significantly following the breed time.The hypercholesteremia influenced synthesis of NO.NO play a key role on motility function of SO.In conclusion,hypercholesteremia and cholecystectomy had an excitation influence on the SO motility in our experiment on rabbits,which might be explained by influencing inhibitory neuron.NO play an important role in the function of SO as an inhibitory neurotransmitter.Once the gallbladder was resected,SO motility reinforced abnormally.It is supposed that the same phenomenon exist clinically.Therefore,prospective,double-blind and control project based on this study is necessary to select those suspected SOD patients who had biliary dyskenisia.