犬Oddi括约肌狭窄模型的建立及其胆道动力学和电生理改变的实验研究
发布时间：2018-08-15 18:48
【摘要】： 背景 Oddi括约肌(SO)是位于胆管、胰管和十二指肠结合部位的神经肌肉复合体,是胆汁和胰液的最终流出道。Oddi括约肌功能障碍(sphincter of Oddi dysfunction, SOD)是目前临床上困扰着患者和医生的一种常见疾病,是胆囊切除术后腹痛的主要原因,也是一些胆石症患者行内镜下括约肌切开(EST)及胆肠吻合术的主要原因,大多数学者倾向于将其分为SO狭窄和SO功能紊乱两种情况。前者为括约肌的部分或全部狭窄,由慢性炎症和纤维化所致,与胰腺炎、胆道结石所致的乳头损伤、胆总管手术时创伤有关;后者为括约肌高压带的周期性功能阻滞,多是由于括约肌痉挛、肥大或去神经所致。完整的SO结构和正常的运动对调节胆汁分泌、预防胆道感染是至关重要的,随着内镜下SO测压及SO肌电记录技术的发展与进步,对其生理及病理生理状态下的活动开始有了一定的认识,而且随着对良性疾病行EST或胆肠吻合术后返流液具有潜在的促癌活性的逐渐认识,如何准确的鉴别SO狭窄和SO功能紊乱,以及尽可能的保留SO的结构和功能完整成为SOD诊断和治疗的难题。为此,本实验通过模拟临床SO狭窄产生的机制,人为建立犬SO器质性狭窄模型,观察狭窄后犬Oddi括约肌胆道动力学和电生理的变化,总结规律,为相关疾病的临床诊疗实践提供合理的理论依据。 目的 探讨犬Oddi括约肌狭窄模型的建立方法及其对胆道动力学和肌电活动的影响,为临床内镜下SOD的诊断和治疗提供理论依据。 方法 禁食16～18h成年杂种犬麻醉后,超声测量胆总管管径,实验组采用经腹行十二指肠系膜对侧切开十二指肠,寻找乳头,采用自制损伤工具插入胆道人为机械性损伤SO后缝合十二指肠、关腹。术后禁食、抗炎、补液2天,饲养28d。对照组仅行开腹十二指肠切开缝合术,不做损伤,其余操作同实验组。所有动物术前和术后1、3、7、14、28d分别抽血查肝功。检测指标包括:ALT,AST,GGT,ALP,TBIL,DBIL,28d后再次麻醉下行超声测量胆总管管径及开腹行SO测压和肌电测量.最后切取SO及周围组织行病理检查。用压力波形分析软件及肌电图形分析软件对得到的数据进行分析。 结果 实验组术后28d肝功能TBIL、DBIL、GGT、ALP明显高于术前,超声测量胆总管管径高于术前,病理检查发现括约肌组织结构紊乱、纤维化,而对照组均无明显变化。在胆道动力学上,实验组胆总管内压(25.10±8.04)mmHg较对照组(10.95±3.56)mmHg升高(P0.05);试验组SO基础压(36.20±7.34)mmHg较对照组(12.50±3.26)mmHg升高(P0.05);试验组SO收缩幅度(7.69±1.87)mmHg较对照组(22.83±5.77)mmHg降低(P0.05);试验组收缩频率(15.93±2.11)次/分较对照组(5.93±2.52)次/分升高(P0.05);试验组收缩时间(3.34±0.62)S较对照组(6.93±2.51)S缩短(P0.05)。在肌电活动上,实验组SOE快波幅度(22.63±13.45)μV与对照组(54.88±16.23)μV相比幅度降低(P0.05);实验组慢波幅度(21.50±12.04)μV与对照组(38.25±12.02)μV相比幅度降低(P0.05)。试验组快波和慢波频率与对照组相比无明显差异(P0.05)。 结论 1.模拟临床SO狭窄产生机制,用机械损伤的方法成功建立了犬SO狭窄模型,并通过测量胆总管管径,化验肝功能变化,和病理改变验证了模型成功。通过病理分度,解决了制作模型一致性的问题。本模型具有手术简便易操作,重复性好,术后便于管理等诸多优点,是用于本课题实验的稳定可靠的研究平台。 2.在SOM方面:与对照组相比,SO器质性狭窄后胆总管内压、SO基础压均有显著升高,但收缩的幅度则下降,收缩频率增加。我们认为狭窄后胆道梗阻,括约肌纤维化、疤痕化、挛缩造成胆总管内压力和括约肌基础压力的升高,但发生器质性损伤的括约肌组织发生纤维化,其弹性下降,收缩能力低于正常肌纤维组织才造成了SO狭窄后收缩幅度的下降。 3.在SOE方面:与对照组相比,狭窄后测量SOE,快波和慢波幅度均缩小,而频率未发现明显差异。由于SO结构紊乱,纤维化,细胞的直径、细胞的电阻和相邻细胞之间的直接电联系也发生了改变,其兴奋性的产生和传导都受到了影响,是其SOE改变的原因。 4.本实验模拟临床SO狭窄产生的机制,成功制作了SO狭窄模型,并就胆道动力学和SO肌电变化做了初步探讨,为临床上SO器质性狭窄和功能性紊乱的鉴别诊断提供了一些实验基础。
[Abstract]:background
Sphincter of Oddi dysfunction (SOD) is a common clinical disorder that troubles patients and doctors. It is the main cause of abdominal pain after cholecystectomy. Endoscopic sphincterotomy (EST) and choledochojejunostomy are the main causes of some cholelithiasis patients. Most scholars tend to classify them into SO stenosis and SO dysfunction. The former is partial or total sphincter stenosis, caused by chronic inflammation and fibrosis, papillary injury caused by pancreatitis, bile duct stones, and common bile duct dysfunction. Trauma is associated with surgery; the latter is a periodic functional block of the sphincter's high-pressure zone, mostly caused by spasm, hypertrophy or denervation of the sphincter. Complete SO structure and normal exercise are essential for regulating bile secretion and preventing biliary tract infection. With the development and progress of endoscopic SO manometry and electromyographic recording techniques, their physiology has been improved. And the activities under the pathophysiological condition have been recognized. With the gradual recognition of the potential tumor-promoting activity of the reflux fluid after EST or cholangioenterostomy in benign diseases, how to accurately identify SO stenosis and SO dysfunction, and how to preserve the structure and function of SO as much as possible become a difficult problem in the diagnosis and treatment of SOD. In this study, the mechanism of SO stenosis was simulated, and the model of SO organic stenosis was established artificially. The changes of biliary tract dynamics and electrophysiology in Oddi sphincter were observed after stenosis, and the regularities were summarized, which provided a reasonable theoretical basis for clinical diagnosis and treatment of related diseases.
objective
Objective To investigate the establishment of Oddi sphincter stenosis model in dogs and its effect on biliary dynamics and electromyographic activity, so as to provide theoretical basis for the diagnosis and treatment of SOD under clinical endoscopy.
Method
The common bile duct diameter was measured by ultrasonography after 16-18 h fasting anesthesia in adult mongrel dogs. The duodenum was incised contralateral to the mesentery via abdomen in the experimental group. The nipples were found. The duodenum was sutured with self-made injury tools after SO mechanical injury of the biliary tract. The abdomen was closed. Duodenostomy and suture were performed without injury, and the other operations were the same as the experimental group. Blood samples were taken before operation and 1, 3, 7, 14 and 28 days after operation to examine liver function. The data were analyzed by pressure wave analysis software and EMG graphic analysis software.
Result
TBIL, DBIL, GGT and ALP of the experimental group were significantly higher than those of the preoperative group on the 28th day after operation. The diameter of the common bile duct measured by ultrasonography was higher than that of the preoperative group. Histological examination showed that the sphincter was disorganized and fibrotic, but there was no significant change in the control group. The basal SO pressure (36.20 (7.34) mmHg in the test group was higher than that in the control group (12.50 (3.26) mmHg (P 0.05); the SO contraction amplitude (7.69 (1.87) mmHg in the test group was lower than that in the control group (22.83 (5.77) mmHg (P 0.05); the systolic frequency (15.93 (2.11) times / score in the test group was higher than that in the control group (5.93 (2.52)/ (P 0.05); the systolic S shortened (P 0.05). In the EMG activity, the amplitude of SOE fast wave (22.63 6550
conclusion
1. To simulate the mechanism of SO stenosis in clinic, a canine model of SO stenosis was successfully established by mechanical injury. The model was proved to be successful by measuring the diameter of common bile duct, examining the changes of liver function and pathological changes. The consistency of the model was solved by pathological grading. The model was simple and easy to operate with good repeatability. It is convenient for management and many other advantages. It is a stable and reliable research platform for this subject experiment.
2. In SO: Compared with the control group, the pressure of common bile duct and the basal pressure of SO increased significantly after SO organic stenosis, but the amplitude of contraction decreased and the frequency of contraction increased. The sphincter of SO stenosis is caused by fibrosis, decreased elasticity and lower contractility than normal muscle fibers.
3. In SOE: Compared with the control group, the amplitude of SOE measured after stenosis was reduced, but the frequency was not significantly different. Because of SO structural disorder, fibrosis, cell diameter, cell resistance and direct electrical connection between adjacent cells also changed, the excitability of SOE production and transmission were affected. The reason.
4. This study simulated the mechanism of SO stenosis in clinic, successfully made SO stenosis model, and made a preliminary study on biliary dynamics and SO EMG changes, providing some experimental basis for clinical differential diagnosis of SO organic stenosis and functional disorders.
【学位授予单位】：第三军医大学
【学位级别】：硕士
【学位授予年份】：2007
【分类号】：R657.4;R-332
本文编号：2185089
[Abstract]:background
Sphincter of Oddi dysfunction (SOD) is a common clinical disorder that troubles patients and doctors. It is the main cause of abdominal pain after cholecystectomy. Endoscopic sphincterotomy (EST) and choledochojejunostomy are the main causes of some cholelithiasis patients. Most scholars tend to classify them into SO stenosis and SO dysfunction. The former is partial or total sphincter stenosis, caused by chronic inflammation and fibrosis, papillary injury caused by pancreatitis, bile duct stones, and common bile duct dysfunction. Trauma is associated with surgery; the latter is a periodic functional block of the sphincter's high-pressure zone, mostly caused by spasm, hypertrophy or denervation of the sphincter. Complete SO structure and normal exercise are essential for regulating bile secretion and preventing biliary tract infection. With the development and progress of endoscopic SO manometry and electromyographic recording techniques, their physiology has been improved. And the activities under the pathophysiological condition have been recognized. With the gradual recognition of the potential tumor-promoting activity of the reflux fluid after EST or cholangioenterostomy in benign diseases, how to accurately identify SO stenosis and SO dysfunction, and how to preserve the structure and function of SO as much as possible become a difficult problem in the diagnosis and treatment of SOD. In this study, the mechanism of SO stenosis was simulated, and the model of SO organic stenosis was established artificially. The changes of biliary tract dynamics and electrophysiology in Oddi sphincter were observed after stenosis, and the regularities were summarized, which provided a reasonable theoretical basis for clinical diagnosis and treatment of related diseases.
objective
Objective To investigate the establishment of Oddi sphincter stenosis model in dogs and its effect on biliary dynamics and electromyographic activity, so as to provide theoretical basis for the diagnosis and treatment of SOD under clinical endoscopy.
Method
The common bile duct diameter was measured by ultrasonography after 16-18 h fasting anesthesia in adult mongrel dogs. The duodenum was incised contralateral to the mesentery via abdomen in the experimental group. The nipples were found. The duodenum was sutured with self-made injury tools after SO mechanical injury of the biliary tract. The abdomen was closed. Duodenostomy and suture were performed without injury, and the other operations were the same as the experimental group. Blood samples were taken before operation and 1, 3, 7, 14 and 28 days after operation to examine liver function. The data were analyzed by pressure wave analysis software and EMG graphic analysis software.
Result
TBIL, DBIL, GGT and ALP of the experimental group were significantly higher than those of the preoperative group on the 28th day after operation. The diameter of the common bile duct measured by ultrasonography was higher than that of the preoperative group. Histological examination showed that the sphincter was disorganized and fibrotic, but there was no significant change in the control group. The basal SO pressure (36.20 (7.34) mmHg in the test group was higher than that in the control group (12.50 (3.26) mmHg (P 0.05); the SO contraction amplitude (7.69 (1.87) mmHg in the test group was lower than that in the control group (22.83 (5.77) mmHg (P 0.05); the systolic frequency (15.93 (2.11) times / score in the test group was higher than that in the control group (5.93 (2.52)/ (P 0.05); the systolic S shortened (P 0.05). In the EMG activity, the amplitude of SOE fast wave (22.63 6550
conclusion
1. To simulate the mechanism of SO stenosis in clinic, a canine model of SO stenosis was successfully established by mechanical injury. The model was proved to be successful by measuring the diameter of common bile duct, examining the changes of liver function and pathological changes. The consistency of the model was solved by pathological grading. The model was simple and easy to operate with good repeatability. It is convenient for management and many other advantages. It is a stable and reliable research platform for this subject experiment.
2. In SO: Compared with the control group, the pressure of common bile duct and the basal pressure of SO increased significantly after SO organic stenosis, but the amplitude of contraction decreased and the frequency of contraction increased. The sphincter of SO stenosis is caused by fibrosis, decreased elasticity and lower contractility than normal muscle fibers.
3. In SOE: Compared with the control group, the amplitude of SOE measured after stenosis was reduced, but the frequency was not significantly different. Because of SO structural disorder, fibrosis, cell diameter, cell resistance and direct electrical connection between adjacent cells also changed, the excitability of SOE production and transmission were affected. The reason.
4. This study simulated the mechanism of SO stenosis in clinic, successfully made SO stenosis model, and made a preliminary study on biliary dynamics and SO EMG changes, providing some experimental basis for clinical differential diagnosis of SO organic stenosis and functional disorders.
【学位授予单位】：第三军医大学
【学位级别】：硕士
【学位授予年份】：2007
【分类号】：R657.4;R-332
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1 李宝山;犬Oddi括约肌狭窄模型的建立及其胆道动力学和电生理改变的实验研究[D];第三军医大学;2007年
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