Bolognesi Massimo, Di Pascoli Marco, Verardo Alberto, Gatta Angelo
Massimo Bolognesi, Marco Di Pascoli, Alberto Verardo, Angelo Gatta, Department of Internal Medicine-DIMED, University of Padua, Azienda Ospedaliera Università di Padova, 35128 Padova, Italy.
World J Gastroenterol. 2014 Mar 14;20(10):2555-63. doi: 10.3748/wjg.v20.i10.2555.
Portal hypertension is a clinical syndrome which leads to several clinical complications, such as the formation and rupture of esophageal and/or gastric varices, ascites, hepatic encephalopathy and hepato-renal syndrome. In cirrhosis, the primary cause of the increase in portal pressure is the enhanced resistance to portal outflow. However, also an increase in splanchnic blood flow worsens and maintains portal hypertension. The vasodilatation of arterial splanchnic vessels and the opening of collateral circulation are the determinants of the increased splanchnic blood flow. Several vasoactive systems/substances, such as nitric oxide, cyclooxygenase-derivatives, carbon monoxide and endogenous cannabinoids are activated in portal hypertension and are responsible for the marked splanchnic vasodilatation. Moreover, an impaired reactivity to vasoconstrictor systems, such as the sympathetic nervous system, vasopressin, angiotensin II and endothelin-1, plays a role in this process. The opening of collateral circulation occurs through the reperfusion and dilatation of preexisting vessels, but also through the generation of new vessels. Splanchnic vasodilatation leads to the onset of the hyperdynamic circulatory syndrome, a syndrome which occurs in patients with portal hypertension and is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure. Understanding the pathophysiology of splanchnic vasodilatation and hyperdynamic circulatory syndrome is mandatory for the prevention and treatment of portal hypertension and its severe complications.
门静脉高压是一种临床综合征，可导致多种临床并发症，如食管和/或胃静脉曲张的形成与破裂、腹水、肝性脑病和肝肾综合征。在肝硬化中，门静脉压力升高的主要原因是门静脉流出阻力增强。然而，内脏血流量增加也会加重并维持门静脉高压。内脏动脉血管扩张和侧支循环开放是内脏血流量增加的决定因素。在门静脉高压时，多种血管活性系统/物质，如一氧化氮、环氧化酶衍生物、一氧化碳和内源性大麻素被激活，并导致显著的内脏血管扩张。此外，对血管收缩系统，如交感神经系统、血管加压素、血管紧张素II和内皮素-1的反应性受损在这一过程中也起作用。侧支循环开放是通过既有血管的再灌注和扩张，也通过新血管的生成实现的。内脏血管扩张导致高动力循环综合征的发生，该综合征发生于门静脉高压患者，其特征为心输出量和心率增加，全身血管阻力降低伴动脉血压降低。了解内脏血管扩张和高动力循环综合征的病理生理学对于门静脉高压及其严重并发症的预防和治疗至关重要。
