Grancea-Iancu M
Department of Internal Medicine and Rheumatology, "Dr. I. Cantacuzino" Hospital; "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania.
J Med Life. 2014;7 Spec No. 3(Spec Iss 3):40-3.
Cirrhosis is a pathological entity characterized by the association of hepatocyte necrosis, fibrosis and regenerative nodules; hemodynamic and neurohormonal metabolic factors intervening in its development mechanisms, resulting in hepatic stellate cell activation and transformation and development of liver fibrosis. Cytokines are key modulators of liver cell fibroblast transformation. Prostaglandins play an important role in the control of vascular tone and in thrombosis; Angiotensin II stimulates fibroblast proliferation by AT-1 receptors. Thrombin influences cellular remodeling in the liver and cardiovascular cirrhotic patients. Oxidative stress is involved in the development of liver cirrhosis by primary and secondary biological irreversible effects. Complex etiology involving vasoactive substances, oxidative stress in the pathogenesis of liver cirrhosis, require further studies to elucidate the mechanisms involved in hemodynamic disturbances associated with this disorder.
肝硬化是一种以肝细胞坏死、纤维化和再生结节相关联为特征的病理实体;血流动力学和神经激素代谢因素参与其发病机制,导致肝星状细胞活化以及肝纤维化的形成和发展。细胞因子是肝细胞成纤维细胞转化的关键调节因子。前列腺素在血管张力控制和血栓形成中起重要作用;血管紧张素II通过AT-1受体刺激成纤维细胞增殖。凝血酶影响肝硬化患者肝脏和心血管系统的细胞重塑。氧化应激通过原发性和继发性生物学不可逆效应参与肝硬化的发展。涉及血管活性物质、氧化应激的复杂病因在肝硬化发病机制中的作用,需要进一步研究以阐明与该疾病相关的血流动力学紊乱所涉及的机制。