Starzl T E, Porter K A, Francavilla A
Curr Probl Surg. 1983 Nov;20(11):687-752. doi: 10.1016/s0011-3840(83)80010-0.
In all species so far studied, including man, portacaval shunt causes the same changes in liver morphology, including hepatocyte atrophy, fatty infiltration, deglycogenation, depletion and disorganization of the rough endoplasmic reticulum (RER) and its lining polyribosomes, and variable but less specific damage to other organelles. Many, perhaps all, biosynthetic processes are quickly depressed, largely secondary to the selective damage to the RER, which is the "factory" of the cell. These structural and metabolic changes in the liver after portal diversion are caused by the diversion around the liver of the hepatotrophic substances in portal venous blood, of which endogenous insulin is the most important. In experimental animals, the injury of Eck's fistula can be prevented by infusing insulin into the tied-off hilar portal vein. The subtle but far-reaching changes in hepatic function after portal diversion have made it possible to use this procedure in palliating three inborn errors of metabolism: glycogen storage disease, familial hypercholesterolemia, and alpha 1-antitrypsin deficiency. In these three diseases, the abnormalities caused by portal diversion have counteracted abnormalities in the patients that were caused by the inborn errors. In these diseases, amelioration of the inborn errors depends on the completeness of the portal diversion. In contrast, total portal diversion to treat complications of portal hypertension is undesirable and always will degrade hepatic function if a significant amount of hepatopetal portal venous blood is taken from the liver. When total portal diversion is achieved (and this is to be expected after all conventional shunts), the incidence of hepatic failure and hepatic encephalopathy is increased. If portal diversion must be done for the control of variceal hemorrhage, a selective procedure such as the Warren procedure is theoretically superior to the completely diverting shunt. In practice, better patient survival has not been achieved after selective shunts than after conventional shunts, but the incidence of hepatic encephalopathy has been less.
在迄今所研究的所有物种（包括人类）中，门腔分流都会引起肝脏形态学上相同的变化，包括肝细胞萎缩、脂肪浸润、糖原脱失、粗面内质网（RER）及其内衬多核糖体的耗竭和紊乱，以及对其他细胞器的不同程度但特异性较低的损伤。许多（或许所有）生物合成过程会迅速受到抑制，这在很大程度上继发于对作为细胞“工厂”的RER的选择性损伤。门静脉分流后肝脏的这些结构和代谢变化是由门静脉血中肝营养物质绕过肝脏分流所致，其中内源性胰岛素最为重要。在实验动物中，通过向结扎的肝门门静脉内输注胰岛素可预防艾克瘘的损伤。门静脉分流后肝脏功能发生的细微但影响深远的变化，使得该手术可用于缓解三种先天性代谢缺陷：糖原贮积病、家族性高胆固醇血症和α1-抗胰蛋白酶缺乏症。在这三种疾病中，门静脉分流引起的异常抵消了患者因先天性缺陷所导致的异常。在这些疾病中，先天性缺陷的改善取决于门静脉分流的彻底程度。相比之下，为治疗门静脉高压并发症而进行的全门静脉分流是不可取的，如果从肝脏抽取大量向肝的门静脉血，总会导致肝功能下降。当实现全门静脉分流时（所有传统分流术后都可预期会出现这种情况），肝衰竭和肝性脑病的发生率会增加。如果必须进行门静脉分流以控制曲张静脉出血，理论上门静脉选择性分流术（如沃伦手术）优于完全分流性分流术。实际上，选择性分流术后患者的生存率并未比传统分流术后更高，但肝性脑病的发生率较低。
