Li Tao, Yang Zhen
Department of General Surgery, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China.
World J Gastroenterol. 2005 Oct 21;11(39):6079-84. doi: 10.3748/wjg.v11.i39.6079.
Portal hypertension, one of the vascular diseases, not only has lesions in liver, but also changes in vascular structures and functions of extrahepatic portal system, systemic system and pulmonary circulation. The pathological changes of vasculopathy in portal hypertension include remodeling of arterialized visceral veins, intimal injury of visceral veins and destruction of contractile structure in visceral arterial wall. The mechanisms of vasculopathy in portal hypertension may be attributed to the changes of hemodynamics in portal system, immune response, gene modulation, vasoactive substances, and intrahepatic blood flow resistance. Portal hypertension can cause visceral hyperdynamic circulation, and the development and progression of visceral vasculopathy, while visceral vasculopathy can promote the development and progression of portal hypertension and visceral hyperdynamic circulation in turn. The aforementioned three factors interact in the pathogenesis of hepatic cirrhosis-induced portal hypertension and are involved in hemorrhage due to varicose vein rupture.
门静脉高压是一种血管疾病，不仅肝脏存在病变，肝外门静脉系统、全身系统及肺循环的血管结构和功能也会发生改变。门静脉高压时血管病变的病理变化包括内脏静脉动脉化重塑、内脏静脉内膜损伤以及内脏动脉壁收缩结构破坏。门静脉高压时血管病变的机制可能归因于门静脉系统血流动力学改变、免疫反应、基因调控、血管活性物质及肝内血流阻力。门静脉高压可导致内脏高动力循环以及内脏血管病变的发生和进展，而内脏血管病变又可反过来促进门静脉高压和内脏高动力循环的发展和进展。上述三个因素在肝硬化所致门静脉高压的发病机制中相互作用，并参与静脉曲张破裂出血。
