Behar J
Rhode Island Hospital and Brown University School of Medicine, Division of Gastroenterology, 593 Eddy Street, Providence, RI 02903, USA.
Curr Gastroenterol Rep. 1999 Apr;1(2):91-4. doi: 10.1007/s11894-996-0005-9.
Impaired gallbladder motility plays an important role in the pathogenesis of benign gallbladder disorders. Defective gallbladder muscle contraction is associated with supersaturated bile with cholesterol and with pregnancy due to high circulating levels of progesterone. These abnormalities result in bile stasis that facilitates gallstone growth. A defective gallbladder muscle contraction may also contribute to the pathogenesis of acute and chronic cholecystitis. In addition, an impaired gallbladder contraction may be the source of recurrent biliary colicky pain in patients with acalculus gallbladder disease. The gallbladders of these patients have an abnormal ejection fraction of less than 35% in response to an intravenous infusion of cholecystokinin (CCK). Although histology of the gallbladder wall is grossly normal, the muscle cells are functionally abnormal, with an impaired response to agonists that act on membrane and cytosolic receptors.
胆囊运动功能受损在良性胆囊疾病的发病机制中起重要作用。胆囊肌肉收缩功能缺陷与胆固醇过饱和胆汁以及因孕酮循环水平升高导致的妊娠有关。这些异常会导致胆汁淤积，从而促进胆结石的生长。胆囊肌肉收缩功能缺陷也可能导致急慢性胆囊炎的发病。此外，胆囊收缩功能受损可能是无结石性胆囊疾病患者反复出现胆绞痛的原因。这些患者的胆囊在静脉注射胆囊收缩素（CCK）后，射血分数异常低于35%。尽管胆囊壁的组织学大体正常，但肌肉细胞功能异常，对作用于膜受体和胞质受体的激动剂反应受损。
