肝硬化患者胆囊排空功能的变化机制探讨  

The Study on the Changes of Gallbladder Emptying and Its Mechanism in Cirrhotics

作　　者：吕静[1] 肖小炜[1] 张永刚[1] 

机构地区：[1]江汉油田总医院,湖北潜江433124

出　　处：《基层医学论坛（B版）》2006年第7期579-580,共2页Public Medical Forum Magazine

摘　　要：目的探讨肝硬化患者胆囊排空功能的变化及其机制。方法B超测定92例肝硬化患者空腹和脂肪餐后胆囊的容积,计算其排空率,并检测血浆胆囊收缩素(CCK)和血管活性肠肽(VIP)的含量,以32例健康人为对照组。结果对照组和ChildA、ChildB、ChildC级肝硬化患者脂肪餐后1小时胆囊排空率依次为(75.3±2.6)%、(63.4±1.9)%、(55.0±0.7)%和(41.1±1.1)%,逐级比较P<0.05;肝硬化患者空腹、餐后血浆CCK和VIP的浓度均高于对照组(P<0.05)。结论肝硬化患者胆囊排空率明显低于对照组,并且肝功损害越重,胆囊排空率越低,其机制可能与CCK和VIP受体发生改变有关。Objective To study the changes of the gallbladder emptying and its mechanism. Methods The gallbladder＇s pre -and postprandial volumes in 92 cirrhotics and 32 controls are checked by B-ultrasonic,and their postprandial gallbladder emptying rates （PGER） are calculated respectively and the plasma levels of CCK and VIP are measure＆ Results PGER in controls, patients with Child A, Child B and Child C respectively are （75.3 ± 2.6）% ,（63.4 ± 1.9）% ,（55.0 ± 0.7）% and （41.1 ± 1.1）% respectively （P〈0.05）;The pre-and postprandial plasm CCK and VIP are higher than those of controls.Conclusion The PGER in cirrhotics is markedly lower than those of controls,Moreover, the more advanced cirrotics,the lowser the PGER is,Which may be related to the receptor changes of CCK and VIP.

关 键 词：肝硬化 胆囊排空 胆囊收缩素 血管活性肠肽 

分 类 号：R657.42[医药卫生—外科学]