犬Oddi括約肌狹窄模型的建立及其膽道動(dòng)力學(xué)和電生理改變的實(shí)驗(yàn)研究
發(fā)布時(shí)間：2018-08-15 18:48
【摘要】： 背景 Oddi括約肌(SO)是位于膽管、胰管和十二指腸結(jié)合部位的神經(jīng)肌肉復(fù)合體,是膽汁和胰液的最終流出道。Oddi括約肌功能障礙(sphincter of Oddi dysfunction, SOD)是目前臨床上困擾著患者和醫(yī)生的一種常見(jiàn)疾病,是膽囊切除術(shù)后腹痛的主要原因,也是一些膽石癥患者行內(nèi)鏡下括約肌切開(kāi)(EST)及膽腸吻合術(shù)的主要原因,大多數(shù)學(xué)者傾向于將其分為SO狹窄和SO功能紊亂兩種情況。前者為括約肌的部分或全部狹窄,由慢性炎癥和纖維化所致,與胰腺炎、膽道結(jié)石所致的乳頭損傷、膽總管手術(shù)時(shí)創(chuàng)傷有關(guān);后者為括約肌高壓帶的周期性功能阻滯,多是由于括約肌痙攣、肥大或去神經(jīng)所致。完整的SO結(jié)構(gòu)和正常的運(yùn)動(dòng)對(duì)調(diào)節(jié)膽汁分泌、預(yù)防膽道感染是至關(guān)重要的,隨著內(nèi)鏡下SO測(cè)壓及SO肌電記錄技術(shù)的發(fā)展與進(jìn)步,對(duì)其生理及病理生理狀態(tài)下的活動(dòng)開(kāi)始有了一定的認(rèn)識(shí),而且隨著對(duì)良性疾病行EST或膽腸吻合術(shù)后返流液具有潛在的促癌活性的逐漸認(rèn)識(shí),如何準(zhǔn)確的鑒別SO狹窄和SO功能紊亂,以及盡可能的保留SO的結(jié)構(gòu)和功能完整成為SOD診斷和治療的難題。為此,本實(shí)驗(yàn)通過(guò)模擬臨床SO狹窄產(chǎn)生的機(jī)制,人為建立犬SO器質(zhì)性狹窄模型,觀察狹窄后犬Oddi括約肌膽道動(dòng)力學(xué)和電生理的變化,總結(jié)規(guī)律,為相關(guān)疾病的臨床診療實(shí)踐提供合理的理論依據(jù)。 目的 探討犬Oddi括約肌狹窄模型的建立方法及其對(duì)膽道動(dòng)力學(xué)和肌電活動(dòng)的影響,為臨床內(nèi)鏡下SOD的診斷和治療提供理論依據(jù)。 方法 禁食16～18h成年雜種犬麻醉后,超聲測(cè)量膽總管管徑,實(shí)驗(yàn)組采用經(jīng)腹行十二指腸系膜對(duì)側(cè)切開(kāi)十二指腸,尋找乳頭,采用自制損傷工具插入膽道人為機(jī)械性損傷SO后縫合十二指腸、關(guān)腹。術(shù)后禁食、抗炎、補(bǔ)液2天,飼養(yǎng)28d。對(duì)照組僅行開(kāi)腹十二指腸切開(kāi)縫合術(shù),不做損傷,其余操作同實(shí)驗(yàn)組。所有動(dòng)物術(shù)前和術(shù)后1、3、7、14、28d分別抽血查肝功。檢測(cè)指標(biāo)包括:ALT,AST,GGT,ALP,TBIL,DBIL,28d后再次麻醉下行超聲測(cè)量膽總管管徑及開(kāi)腹行SO測(cè)壓和肌電測(cè)量.最后切取SO及周?chē)M織行病理檢查。用壓力波形分析軟件及肌電圖形分析軟件對(duì)得到的數(shù)據(jù)進(jìn)行分析。 結(jié)果 實(shí)驗(yàn)組術(shù)后28d肝功能TBIL、DBIL、GGT、ALP明顯高于術(shù)前,超聲測(cè)量膽總管管徑高于術(shù)前,病理檢查發(fā)現(xiàn)括約肌組織結(jié)構(gòu)紊亂、纖維化,而對(duì)照組均無(wú)明顯變化。在膽道動(dòng)力學(xué)上,實(shí)驗(yàn)組膽總管內(nèi)壓(25.10±8.04)mmHg較對(duì)照組(10.95±3.56)mmHg升高(P0.05);試驗(yàn)組SO基礎(chǔ)壓(36.20±7.34)mmHg較對(duì)照組(12.50±3.26)mmHg升高(P0.05);試驗(yàn)組SO收縮幅度(7.69±1.87)mmHg較對(duì)照組(22.83±5.77)mmHg降低(P0.05);試驗(yàn)組收縮頻率(15.93±2.11)次/分較對(duì)照組(5.93±2.52)次/分升高(P0.05);試驗(yàn)組收縮時(shí)間(3.34±0.62)S較對(duì)照組(6.93±2.51)S縮短(P0.05)。在肌電活動(dòng)上,實(shí)驗(yàn)組SOE快波幅度(22.63±13.45)μV與對(duì)照組(54.88±16.23)μV相比幅度降低(P0.05);實(shí)驗(yàn)組慢波幅度(21.50±12.04)μV與對(duì)照組(38.25±12.02)μV相比幅度降低(P0.05)。試驗(yàn)組快波和慢波頻率與對(duì)照組相比無(wú)明顯差異(P0.05)。 結(jié)論 1.模擬臨床SO狹窄產(chǎn)生機(jī)制,用機(jī)械損傷的方法成功建立了犬SO狹窄模型,并通過(guò)測(cè)量膽總管管徑,化驗(yàn)肝功能變化,和病理改變驗(yàn)證了模型成功。通過(guò)病理分度,解決了制作模型一致性的問(wèn)題。本模型具有手術(shù)簡(jiǎn)便易操作,重復(fù)性好,術(shù)后便于管理等諸多優(yōu)點(diǎn),是用于本課題實(shí)驗(yàn)的穩(wěn)定可靠的研究平臺(tái)。 2.在SOM方面:與對(duì)照組相比,SO器質(zhì)性狹窄后膽總管內(nèi)壓、SO基礎(chǔ)壓均有顯著升高,但收縮的幅度則下降,收縮頻率增加。我們認(rèn)為狹窄后膽道梗阻,括約肌纖維化、疤痕化、攣縮造成膽總管內(nèi)壓力和括約肌基礎(chǔ)壓力的升高,但發(fā)生器質(zhì)性損傷的括約肌組織發(fā)生纖維化,其彈性下降,收縮能力低于正常肌纖維組織才造成了SO狹窄后收縮幅度的下降。 3.在SOE方面:與對(duì)照組相比,狹窄后測(cè)量SOE,快波和慢波幅度均縮小,而頻率未發(fā)現(xiàn)明顯差異。由于SO結(jié)構(gòu)紊亂,纖維化,細(xì)胞的直徑、細(xì)胞的電阻和相鄰細(xì)胞之間的直接電聯(lián)系也發(fā)生了改變,其興奮性的產(chǎn)生和傳導(dǎo)都受到了影響,是其SOE改變的原因。 4.本實(shí)驗(yàn)?zāi)M臨床SO狹窄產(chǎn)生的機(jī)制,成功制作了SO狹窄模型,并就膽道動(dòng)力學(xué)和SO肌電變化做了初步探討,為臨床上SO器質(zhì)性狹窄和功能性紊亂的鑒別診斷提供了一些實(shí)驗(yàn)基礎(chǔ)。
[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.
【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2007
【分類(lèi)號(hào)】：R657.4;R-332
本文編號(hào)：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.
【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2007
【分類(lèi)號(hào)】：R657.4;R-332
【相似文獻(xiàn)】
相關(guān)碩士學(xué)位論文 前1條
1 李寶山;犬Oddi括約肌狹窄模型的建立及其膽道動(dòng)力學(xué)和電生理改變的實(shí)驗(yàn)研究[D];第三軍醫(yī)大學(xué);2007年
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