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胆道运动功能障碍。

Biliary tract motor dysfunction.

作者信息

Toouli J

出版信息

Baillieres Clin Gastroenterol. 1991 Jun;5(2):409-30. doi: 10.1016/0950-3528(91)90035-y.

DOI:10.1016/0950-3528(91)90035-y
PMID:1912657
Abstract

Gallbladder and sphincter of Oddi motility regulates the flow of bile from the liver to the duodenum. During the interdigestive period most secreted bile is diverted into the gallbladder where it is concentrated, but a significant minority of the biliary secretion passes directly into the duodenum. Regulation of this flow is mainly via the phasic contractions of the sphincter of Oddi and the sphincter basal tone. The phasic contractions expel small volumes of fluid into the duodenum, but most of the flow occurs between the contractions and is therefore not dependent on peristaltic pumping, but rather on a small pressure gradient. During fasting, just prior to duodenal phase III activity, the gallbladder expels up to 40% of its volume and the sphincter phasic contractions increase. Following a meal, the gallbladder empties its contents, and the sphincter of Oddi resistance is reduced via a fall in basal pressure and inhibition of the amplitude of phasic contractions. Control of this activity is via an interplay of both neuronal and hormonal factors which together have an effect on both gallbladder and sphincter of Oddi motility. Abnormalities in motility are recognized for both the gallbladder and the sphincter of Oddi. Gallbladder dyskinesia is objectively diagnosed using the radionuclide GBEF. In patients with a GBEF less than 40% cholecystectomy results in relief of symptoms. In postcholecystectomy patients sphincter of Oddi dysfunction presents as either biliary-like pain or idiopathic recurrent pancreatitis. Endoscopic sphincter of Oddi manometry provides the most objective diagnostic information. In patients with a sphincter of Oddi stenosis, characterized manometrically as an elevated basal pressure, division of the sphincter results in relief of symptoms. For patients with biliary-like pain, division is performed as an endoscopic sphincterotomy, whereas for patients with idiopathic recurrent pancreatitis, a sphincteroplasty and pancreatic duct septectomy are required.

摘要

胆囊和Oddi括约肌的运动调节胆汁从肝脏到十二指肠的流动。在消化间期,大部分分泌的胆汁被转移到胆囊中进行浓缩,但一小部分胆汁分泌直接进入十二指肠。这种流动的调节主要通过Oddi括约肌的阶段性收缩和括约肌基础张力。阶段性收缩将少量液体排入十二指肠,但大部分流动发生在收缩之间,因此不依赖于蠕动泵,而是依赖于一个小的压力梯度。在禁食期间,就在十二指肠第三期活动之前,胆囊排出其容量的40%,括约肌的阶段性收缩增加。进食后,胆囊排空其内容物,Oddi括约肌的阻力通过基础压力下降和阶段性收缩幅度的抑制而降低。这种活动的控制是通过神经和激素因素的相互作用共同影响胆囊和Oddi括约肌的运动。胆囊和Oddi括约肌的运动异常均已得到确认。胆囊运动障碍可通过放射性核素GBEF进行客观诊断。GBEF低于40%的患者行胆囊切除术后症状缓解。在胆囊切除术后的患者中,Oddi括约肌功能障碍表现为胆绞痛样疼痛或特发性复发性胰腺炎。内镜下Oddi括约肌测压提供了最客观的诊断信息。对于以测压特征为基础压力升高的Oddi括约肌狭窄患者,括约肌切开可缓解症状。对于胆绞痛样疼痛的患者,采用内镜括约肌切开术,而对于特发性复发性胰腺炎的患者,则需要进行括约肌成形术和胰管隔膜切除术。

相似文献

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Biliary tract motor dysfunction.胆道运动功能障碍。
Baillieres Clin Gastroenterol. 1991 Jun;5(2):409-30. doi: 10.1016/0950-3528(91)90035-y.
2
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Sphincter of Oddi dysfunction.奥迪括约肌功能障碍
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Fasting canine biliary secretion and the sphincter of Oddi.禁食犬的胆汁分泌与奥迪括约肌。
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[The effect of endoscopic sphincterotomy on the motility of the gallbladder and of the sphincter of Oddi in patients with acalculous biliary pain syndrome].[内镜下括约肌切开术对无结石性胆绞痛综合征患者胆囊及Oddi括约肌运动功能的影响]
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[Gallbladder dyskinesia and manometry of Oddi's sphincter].[胆囊运动障碍与奥狄括约肌测压]
Schweiz Med Wochenschr Suppl. 1993;54:22-5.

引用本文的文献

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2
Effect of nitric oxide on gallbladder motility in patients with acalculous biliary pain: a cholescintigraphic study.一氧化氮对无结石性胆绞痛患者胆囊运动功能的影响:一项胆囊闪烁造影研究
Dig Dis Sci. 2002 Sep;47(9):1975-81. doi: 10.1023/a:1019648123515.
3
Differentiation between organic stenosis and functional dyskinesia of the sphincter of Oddi with amyl nitrite-augmented quantitative hepatobiliary scintigraphy.
亚硝酸异戊酯增强定量肝胆闪烁显像对Oddi括约肌器质性狭窄与功能性运动障碍的鉴别诊断
Eur J Nucl Med. 1994 Mar;21(3):203-8. doi: 10.1007/BF00188666.
4
Evaluation of results of the prostigmine-morphine test with quantitative hepatobiliary scintigraphy: a new method for the diagnosis of sphincter of Oddi dyskinesia.用定量肝胆闪烁扫描术评估新斯的明-吗啡试验结果:诊断Oddi括约肌运动障碍的一种新方法。
Eur J Nucl Med. 1995 Mar;22(3):227-32. doi: 10.1007/BF01081517.