Iwakiri Yasuko, Groszmann Roberto J
Hepatic Hemodynamic Laboratory, VA Connecticut Healthcare System, West Haven, CT 06516, USA.
Hepatology. 2006 Feb;43(2 Suppl 1):S121-31. doi: 10.1002/hep.20993.
The hyperdynamic circulatory syndrome observed in chronic liver diseases is a great example of research that originated from clinical observations and progressed in the last 50 years from the patient to the experimental laboratory. Our knowledge has evolved from the patient to the molecule, using experimental models that serve as a source for understanding the complex pathophysiological mechanisms that govern this complex syndrome. We now know that progressive vasodilatation is central to the detrimental effects observed in multiple organs. Although nitric oxide has been shown to be the primary vasodilator molecule in these effects, other molecules also participate in the complex mechanisms of vasodilatation. This review summarizes three major areas: first, clinical observation in patients; second, experimental models used to study the hyperdynamic circulatory syndrome; and third, the vasodilator molecules that play roles in vascular abnormalities observed in portal hypertension.
在慢性肝病中观察到的高动力循环综合征是一个很好的研究范例，该研究起源于临床观察，并在过去50年里从患者研究发展到实验实验室研究。我们的知识已从患者层面深入到分子层面，借助实验模型来理解调控这一复杂综合征的复杂病理生理机制。我们现在知道，进行性血管舒张是在多个器官中观察到的有害效应的核心。尽管一氧化氮已被证明是这些效应中的主要血管舒张分子，但其他分子也参与了血管舒张的复杂机制。本综述总结了三个主要方面：第一，患者的临床观察；第二，用于研究高动力循环综合征的实验模型；第三，在门静脉高压中观察到的血管异常中发挥作用的血管舒张分子。
