Doty J E, Pitt H A, Kuchenbecker S L, Porter-Fink V, DenBesten L W
Am J Surg. 1983 Jan;145(1):54-61. doi: 10.1016/0002-9610(83)90166-6.
Recent observations indicate that the hepatic secretion of lithogenic bile, gallbladder mucus hypersection, and gallbladder stasis are all critical factors in the pathogenesis of cholesterol gallstones. Using the prairie dog gallstone model, we investigated the interaction of these factors and the sequence in which they develop. The results of this study indicated that (1) gallbladder bile mucus concentration is elevated before cholesterol precipitation and increases progressively with the formation of cholesterol crystals, (2) cystic duct resistance increases in the presence of cholesterol crystals, but not fine, sonicated crystals increase cystic duct resistance. We conclude that these alterations trigger a self-perpetuating cycle of mucus hypersecretion, cholesterol crystallization, and gallbladder stasis which culminates in the formation of cholesterol gallstones.
最近的观察表明,致石性胆汁的肝脏分泌、胆囊黏液过度分泌和胆囊淤滞都是胆固醇性胆结石发病机制中的关键因素。利用草原犬鼠胆结石模型,我们研究了这些因素之间的相互作用以及它们发生发展的顺序。本研究结果表明:(1)胆囊胆汁黏液浓度在胆固醇沉淀之前升高,并随着胆固醇晶体的形成而逐渐增加;(2)在存在胆固醇晶体的情况下胆囊管阻力增加,但微小的、经超声处理的晶体不会增加胆囊管阻力。我们得出结论,这些改变引发了一个黏液过度分泌、胆固醇结晶和胆囊淤滞的自我持续循环,最终导致胆固醇性胆结石的形成。