AIM: The role of the sphincter of Oddi (SO) in ethanol (ETOH)-induced pancreatitis is controversial. Our aim was to characterise the effect of ETOH on basal and stimulated SO motility.METHODS: SOs removed from white r...AIM: The role of the sphincter of Oddi (SO) in ethanol (ETOH)-induced pancreatitis is controversial. Our aim was to characterise the effect of ETOH on basal and stimulated SO motility.METHODS: SOs removed from white rabbits were placed in an organ bath (Krebs solution, pH7.4, 37℃). The effects of 2 mL/L, 4 mL/L, 6 mL/L and 8 mL/L of ETOH on the contractile responses of the sphincter were determined.1 SOs were stimulated with either 0.1μol/L carbachol, 1μol/L erythromycin or 0.1μol/L cholecystokinin (CCK).RESULTS: ETOH at a dose of 4 mL/L significantly decreased the baseline contractile amplitude from 11.98±0.05 mN to 11.19±0.07 mN. However, no significant changes in the contractile frequency were observed. ETOH (0.6%) significantly decreased both the baseline amplitude and the frequency compared to the control group (10.50±0.01 mN,12.13±0.10 mN and 3.53±0.13 c/min, 5.5±0.13 cycles(c)/min,respectively). Moreover, 0.8% of ETOH resulted in complete relaxation of the SO. Carbachol (0.1μol/L)or erythromycin (1μol/L) stimulated the baseline amplitudes (by 82% and 75%, respectively) and the contractile frequencies (by 150% and 106%, respectively). In the carbachol or en/thromydn-stimulated groups 2-6 mL/L of ETOH significantly inhibited both the amplitude and the frequency. Interestingly,a 4-5 min administration of 6 mL/L ETOH suddenly and completely relaxed the SO. CCK (0.1μol/L) stimulated the baseline amplitude from 12.37±0.05 mN to 27.40±1.82 mN within 1.60±0.24 min. After this peak, the amplitudede creased to 17.17±0.22 mN and remained constant during the experiment. The frequency peaked at 12.8±0.2 c/min,after which the constant frequency was 9.43±0.24 c/min throughout the rest of the experiment. ETOH at a dose of 4 mL/L significantly decreased the amplitude from 16.13±0.23 mN to 14.93±0.19 mN. However, no significant changes in the contractile frequency were observed. ETOH at a dose of 6 mL/L inhibited both the amplitudes and the frequencies in the CCK-stimulated group, while 8 mL/L of ETOH completely relaxed the SO.CONCLUSION: ETOH strongly inhibits the basal, carbachol,erythromycin, and CCK-stimulated rabbit SO motility.Therefore, it is possible that during alcohol-intake the relaxed SO opens the way for pancreatic fluid to flow out into the duodenum in rabbits. This relaxation of the SO may protect the pancreas against alcohol-induced damage.展开更多
[目的]了解芍药甙对家兔离体Oddi括约肌(sphincter of Oddi,SO)肌环收缩活动的影响。[方法]制备离体兔Oddi括约肌肌环标本,放置于平滑肌恒温灌流浴槽中,观察累积浓度芍药甙对乙酰胆碱(Ach)预收缩(乙酰胆碱组)的SO肌环的作用和芍药甙对...[目的]了解芍药甙对家兔离体Oddi括约肌(sphincter of Oddi,SO)肌环收缩活动的影响。[方法]制备离体兔Oddi括约肌肌环标本,放置于平滑肌恒温灌流浴槽中,观察累积浓度芍药甙对乙酰胆碱(Ach)预收缩(乙酰胆碱组)的SO肌环的作用和芍药甙对经无钙液(无钙液组)、无钙液加肝素(肝素组)预处理的SO肌环的作用。[结果]当芍药甙浓度累积达(12.5、25、50、100)μmol/L时,对Ach(10-6mol/L)预收缩的SO肌环产生剂量依赖性舒张作用(P<0.05)。经无钙液预处理后,芍药甙(100μmol/L)对SO肌环的舒张作用未被阻断;但经无钙液加肝素预处理后,该作用被明显抑制。[结论]芍药甙对Oddi括约肌具有舒张作用。其机制可能与阻断平滑肌细胞内质网上的三磷酸肌醇敏感的钙离子通道,抑制内钙的释放有关。展开更多
Oddi括约肌(sphincter of Oddi)是一具有复杂生理功能的肌性结构。它的主要功能是调节胆囊充盈,控制胆汁、胰液入十二指肠流量,并防止十二指肠内容物返流入胆胰管以及调控胆胰管内的压力。尽管Oddi括约肌运动功能异常与急性胰腺炎发生...Oddi括约肌(sphincter of Oddi)是一具有复杂生理功能的肌性结构。它的主要功能是调节胆囊充盈,控制胆汁、胰液入十二指肠流量,并防止十二指肠内容物返流入胆胰管以及调控胆胰管内的压力。尽管Oddi括约肌运动功能异常与急性胰腺炎发生的相互关系尚未完全阐明,但研究表明其与急性胰腺炎的发生、发展有密切的联系。本文就Oddi括约肌的运动功能、运动调节、肌电生理活动、以及与急性胰腺炎发生发展的相互关系作一简单综述。展开更多
Gastroesophageal reflux disease (GERD) affects an estimated 20% of the population in the United States. About 10%-15% of patients with GERD develop Barrett’s esophagus, which can progress to adenocarcinoma, currently...Gastroesophageal reflux disease (GERD) affects an estimated 20% of the population in the United States. About 10%-15% of patients with GERD develop Barrett’s esophagus, which can progress to adenocarcinoma, currently the most prevalent type of esophageal cancer. The esophagus is normally lined by squamous mucosa, therefore, it is clear that for adenocarcinoma to develop, there must be a sequence of events that result in transformation of the normal squamous mucosa into columnar epithelium. This sequence begins with gastroesophageal reflux, and with continued injury metaplastic columnar epithelium develops. This article reviews the pathophysiology of Barrett’s esophagus and implications for its treatment. The effect of medical and surgical therapy of Barrett’s esophagus is compared.展开更多
基金Supported by The Wellcome Trust (Grant No.022618),and by the Hungarian Scientific Research Fund (D42188,T43066 and T042589)
文摘AIM: The role of the sphincter of Oddi (SO) in ethanol (ETOH)-induced pancreatitis is controversial. Our aim was to characterise the effect of ETOH on basal and stimulated SO motility.METHODS: SOs removed from white rabbits were placed in an organ bath (Krebs solution, pH7.4, 37℃). The effects of 2 mL/L, 4 mL/L, 6 mL/L and 8 mL/L of ETOH on the contractile responses of the sphincter were determined.1 SOs were stimulated with either 0.1μol/L carbachol, 1μol/L erythromycin or 0.1μol/L cholecystokinin (CCK).RESULTS: ETOH at a dose of 4 mL/L significantly decreased the baseline contractile amplitude from 11.98±0.05 mN to 11.19±0.07 mN. However, no significant changes in the contractile frequency were observed. ETOH (0.6%) significantly decreased both the baseline amplitude and the frequency compared to the control group (10.50±0.01 mN,12.13±0.10 mN and 3.53±0.13 c/min, 5.5±0.13 cycles(c)/min,respectively). Moreover, 0.8% of ETOH resulted in complete relaxation of the SO. Carbachol (0.1μol/L)or erythromycin (1μol/L) stimulated the baseline amplitudes (by 82% and 75%, respectively) and the contractile frequencies (by 150% and 106%, respectively). In the carbachol or en/thromydn-stimulated groups 2-6 mL/L of ETOH significantly inhibited both the amplitude and the frequency. Interestingly,a 4-5 min administration of 6 mL/L ETOH suddenly and completely relaxed the SO. CCK (0.1μol/L) stimulated the baseline amplitude from 12.37±0.05 mN to 27.40±1.82 mN within 1.60±0.24 min. After this peak, the amplitudede creased to 17.17±0.22 mN and remained constant during the experiment. The frequency peaked at 12.8±0.2 c/min,after which the constant frequency was 9.43±0.24 c/min throughout the rest of the experiment. ETOH at a dose of 4 mL/L significantly decreased the amplitude from 16.13±0.23 mN to 14.93±0.19 mN. However, no significant changes in the contractile frequency were observed. ETOH at a dose of 6 mL/L inhibited both the amplitudes and the frequencies in the CCK-stimulated group, while 8 mL/L of ETOH completely relaxed the SO.CONCLUSION: ETOH strongly inhibits the basal, carbachol,erythromycin, and CCK-stimulated rabbit SO motility.Therefore, it is possible that during alcohol-intake the relaxed SO opens the way for pancreatic fluid to flow out into the duodenum in rabbits. This relaxation of the SO may protect the pancreas against alcohol-induced damage.
文摘[目的]了解芍药甙对家兔离体Oddi括约肌(sphincter of Oddi,SO)肌环收缩活动的影响。[方法]制备离体兔Oddi括约肌肌环标本,放置于平滑肌恒温灌流浴槽中,观察累积浓度芍药甙对乙酰胆碱(Ach)预收缩(乙酰胆碱组)的SO肌环的作用和芍药甙对经无钙液(无钙液组)、无钙液加肝素(肝素组)预处理的SO肌环的作用。[结果]当芍药甙浓度累积达(12.5、25、50、100)μmol/L时,对Ach(10-6mol/L)预收缩的SO肌环产生剂量依赖性舒张作用(P<0.05)。经无钙液预处理后,芍药甙(100μmol/L)对SO肌环的舒张作用未被阻断;但经无钙液加肝素预处理后,该作用被明显抑制。[结论]芍药甙对Oddi括约肌具有舒张作用。其机制可能与阻断平滑肌细胞内质网上的三磷酸肌醇敏感的钙离子通道,抑制内钙的释放有关。
文摘Oddi括约肌(sphincter of Oddi)是一具有复杂生理功能的肌性结构。它的主要功能是调节胆囊充盈,控制胆汁、胰液入十二指肠流量,并防止十二指肠内容物返流入胆胰管以及调控胆胰管内的压力。尽管Oddi括约肌运动功能异常与急性胰腺炎发生的相互关系尚未完全阐明,但研究表明其与急性胰腺炎的发生、发展有密切的联系。本文就Oddi括约肌的运动功能、运动调节、肌电生理活动、以及与急性胰腺炎发生发展的相互关系作一简单综述。
文摘Gastroesophageal reflux disease (GERD) affects an estimated 20% of the population in the United States. About 10%-15% of patients with GERD develop Barrett’s esophagus, which can progress to adenocarcinoma, currently the most prevalent type of esophageal cancer. The esophagus is normally lined by squamous mucosa, therefore, it is clear that for adenocarcinoma to develop, there must be a sequence of events that result in transformation of the normal squamous mucosa into columnar epithelium. This sequence begins with gastroesophageal reflux, and with continued injury metaplastic columnar epithelium develops. This article reviews the pathophysiology of Barrett’s esophagus and implications for its treatment. The effect of medical and surgical therapy of Barrett’s esophagus is compared.
