Hennenberg M, Trebicka J, Sauerbruch T, Heller J
Department of Internal Medicine I, University of Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany.
Gut. 2008 Sep;57(9):1300-14. doi: 10.1136/gut.2007.144584. Epub 2008 Apr 29.
In liver cirrhosis, abnormal persistent extrahepatic vasodilation leads to hyperdynamic circulatory dysfunction which essentially contributes to portal hypertension. Since portal hypertension is a major factor in the development of complications in cirrhosis, the mechanisms underlying this vasodilation are of paramount interest. Extensive studies performed in cirrhotic patients and animals revealed that this vasodilation is associated on the one hand with enhanced formation of vasodilators, and on the other hand with vascular hyporesponsiveness to vasoconstrictors. The latter phenomenon has been termed "vascular hypocontractility". It is caused by a combination of different mechanisms and factors described in this review.
在肝硬化中，异常持续的肝外血管扩张导致高动力循环功能障碍，这是门静脉高压的主要成因。由于门静脉高压是肝硬化并发症发生发展的主要因素，这种血管扩张的潜在机制备受关注。对肝硬化患者和动物进行的大量研究表明，这种血管扩张一方面与血管扩张剂生成增加有关，另一方面与血管对血管收缩剂反应性降低有关。后一种现象被称为“血管收缩功能减退”。它是由本综述中描述的多种不同机制和因素共同作用引起的。
