摘要：目的探讨谷氨酰胺(GLN)／胆囊收缩素(CCK)，在完全胃肠外营养(TPN)支持期间预防胆汁瘀积的作用，分别阐明GLN和CCK在预防胆汁瘀积中的作用机制及其相互关系。方法采用新西兰纯种白兔做TPN模型，分为四组，Ⅰ组TPN，Ⅱ组TPN+GLN，Ⅲ组TPN+CCK，Ⅳ组TPN+GLN+CCK。每组各分半数分别观察至四周和八周二个阶段后处死。经过血液生化检查、胆汁成分分析、大体形态观察、光学显微镜观察和电子显微镜扫描，对比观察各组每个阶段有否胆汁瘀积、胆囊形态变化及其程度。结果血液监测Ⅰ组GPT、AKP、直接胆红素和胆固醇在四周时较Ⅱ、Ⅲ、Ⅳ组有升高趋势，第八周时有明显升高。胆汁检验Ⅰ、Ⅱ组第四周时直接胆红素和胆固醇较Ⅲ、Ⅳ组有较明显升高。光镜、电镜扫描示工、Ⅲ组胆囊壁第四周时上皮呈矮柱状、着色逐渐加深、细胞内水肿、线粒体轻度肿胀，第八周时工、Ⅲ组胆囊壁在固有膜和肌层间出现了明显间隙，胞浆混浊，内有较大脂滴，内质网有空泡形成，而Ⅱ、Ⅳ组胆囊壁四周时呈正常细胞器官，八周时Ⅱ组有轻度改变，Ⅳ组仍为正常的细胞器官。结论TPN支持期间确能发生胆汁瘀积，而且时间越长其程度越严重。TPN+GLN可以保护维持胆囊壁组织细胞的完整和功能，但无直接预防胆汁瘀积作用。TPN+CCK具有明显缩胆和促进胆汁排泄作用，但若胆囊壁受损，CCK将失去其作用。TPN+GLN+CCK不仅具有保护和维持胆囊壁组织细胞的完整性和功能，而且还有明显的缩胆囊、促进胆汁排泄的作用，证明是预防TPN支持期间胆汁瘀积的最佳方法。

The role of glutamine and C. C. K in preventing cholestasis during PN

wANG Shengjiang,LIU Liren,MU Haifeng(Forth Affiliated Hospital, Harbin Medical University)

Abstract：Objective Purpose: Study Glutarnine(GLN)/Cholecystokinin (CCK)'s action of preventing cholestasis during total parenteral nutrition(TPN) and detail action mechanism of GLN and CCK and relationship between each other. Methods Adopt Newzealand pure species white hares as TPN models. All hares were divided into four teams, in which 1st team was designated as TPN team, 2nd team as TPN + GLN team, 3rd team as TPN + CCK team, and 4th team as TPN + GLN + CCK team. Each team was divided into two halves in turn. One half were killed after four-week observation and the other half were killed after 8 weeks. Through blood biochemical examination, analysis of chole components, observation of macrostructure, scan of light and esectron microecopes, we observed if there were cholestasis, gallbladder constmctural alteration and its degree. Results Through blood monitoring, increases of gPT. AKP. cholehilirubin and cholesterol were observed in the first team as compared with the second to forth teams at the forth week and higher increases were found at the 8th week. In choletest,cholebilirubin and cholesterol were higher in the first and second teams than in the third and fourth ones at the 4th week and were higher instinctively in the first to third teams than in the forth team at the 8th week. Scan of light and electron microscopes demonstrated that cholepithelia became low-column shape. Dyeing was deepened. There was cytoedema and mitochondrial got swelling at the 4th week in the first and third teams. At the 8th week, there was tissue between lamina propria and muscle layer. Cyto-plasm became muddy, in which there were bigger fatty drops. There were vacuity in cytoreticulum. In the second and forth teams, we found normal cell density at the 4th week. At the 8th week, there was small alteration in the second team and normal density in the forth team. Conclusions It is true that cholestasis will take place during TPN and become serious with time prolonging. Integrality and function of choleeystis, wall tissue cell can be defended and sustained by applying TPN and gLN, but there is no direct preventing action. There are apparent cholecystokinetic and cholagogic functions by applying TPN + cCK. But CASK will lose its function if cholecystis-wall is damaged. There are not only preventing and sustaining functions for the integrality and function of cholecystis-waU tissue cell but also apperent function of chole constriction and cholegogue by applying TPN + GLN + cCK. It is proved to be the best way to prevent cholestasis during. T. P. N.