Shaffer E A
Department of Medicine, University of Calgary, Faculty of Medicine, Foothills Medical Center, Alberta, Canada.
Aliment Pharmacol Ther. 2000 May;14 Suppl 2:2-8. doi: 10.1046/j.1365-2036.2000.014s2002.x.
Muscular contraction of the gall-bladder is the primary determinant of bile delivery into the duodenum. Where bile goes following its secretion by the liver depends upon a co-ordinated series of pressure interrelations between the hepatic secretory pressure at the entrance to the biliary system, a low pressure conduit, and the pressure differences between the gall-bladder, cystic duct and sphincter of Oddi. During fasting, the relatively higher tone in the sphincter of Oddi fosters the entry of bile into the gall-bladder. The gall-bladder accommodates this influx without an increase in intravesicular pressure through its compliance or distensibility, which consists of active muscle relaxation and passive fibroelastic components. The concentrating function of the gall-bladder keeps the volume small. Once about every 120 min during the interdigestive period, gall-bladder emptying occurs coincident with intense duodenal contractions; all part of the migratory myoelectric complex. This helps maintain the enterohepatic circulation of bile salts. Motilin, which mediates these events during fasting, acts by stimulating intrinsic cholinergic nerves. Cholecystokinin is the major determinant of gallbladder emptying with eating. Cholecystokinin acts through pre-ganglionic cholinergic nerves, to initiate gall-bladder contraction. Agonists like cholecystokinin and acetylcholine cause contraction of gall-bladder smooth muscle through signal transduction, which increases intracellular calcium levels and so initiates the contractile machinery. Cholecystokinin also acts on the sphincter of Oddi via pre-ganglionic cholinergic nerves to release vasoactive intestinal polypeptide and nitric oxide, and so lower tone. These events are co-ordinated with motility and secretory events in the upper gastrointestinal tract, delivering bile at appropriate times into the duodenum.
胆囊的肌肉收缩是胆汁排入十二指肠的主要决定因素。肝脏分泌的胆汁去向取决于胆道系统入口处的肝分泌压力（胆道系统是一个低压管道）、胆囊、胆囊管和奥迪括约肌之间一系列相互协调的压力关系。在禁食期间，奥迪括约肌相对较高的张力促使胆汁进入胆囊。胆囊通过其顺应性或扩张性来容纳这种流入，而不会使囊内压力增加，顺应性或扩张性包括主动的肌肉松弛和被动的纤维弹性成分。胆囊的浓缩功能使胆汁体积保持较小。在消化间期，大约每隔120分钟，胆囊排空会与十二指肠强烈收缩同时发生；这都是移行性肌电复合波的一部分。这有助于维持胆盐的肠肝循环。胃动素在禁食期间介导这些事件，其作用是刺激内在胆碱能神经。胆囊收缩素是进食时胆囊排空的主要决定因素。胆囊收缩素通过节前胆碱能神经起作用，引发胆囊收缩。胆囊收缩素和乙酰胆碱等激动剂通过信号转导导致胆囊平滑肌收缩，这会增加细胞内钙水平，从而启动收缩机制。胆囊收缩素还通过节前胆碱能神经作用于奥迪括约肌，释放血管活性肠肽和一氧化氮，从而降低张力。这些事件与上消化道的运动和分泌事件相互协调，在适当的时候将胆汁排入十二指肠。
