Reichen J
Department of Clinical Pharmacology, University of Berne.
Z Gastroenterol. 1988 Sep;26 Suppl 2:3-7.
Portal hypertension may result from increased resistance of the hepatic vascular bed ("backflow") and from a hyperdynamic splanchnic circulation ("forward flow" theory). Most likely, both mechanisms contribute to the formation of portal hypertension in man. The classical macroscopic terminology describes prehepatic, intrahepatic and posthepatic forms of portal hypertension. Increased splanchnic blood flow represents the predominant cause of some pre- and intrahepatic types of portal hypertension. Intrahepatic portal hypertension has been subclassified as presinusoidal, sinusoidal or postsinusoidal. However, one to one allotments of diseases to this classification may not be made. The relative contribution of each of these causes to the increased portal pressure of liver cirrhosis varies with the etiology of the disease. A new ultrastructural classification of the processes leading to portal hypertension differentiates primarily hepatocellular (e.g., increased hepatocellular size) from interstitional causes (e.g., sinusoidal capillarization). The role of the fenestrated sinusoidal endothelial cells in the regulation of intrahepatic resistance and, thus, for the generation of portal hypertension is poorly defined up to date. A thorough evaluation of the effects of prostanglandins, leukotrienes, catecholamines, serotonin and others on sinusoidal endothelial cells and hepatic microcirculation may provide the basis for new therapeutic avenues.
门静脉高压可能源于肝血管床阻力增加（“逆流”）和内脏高动力循环（“顺流”理论）。很可能这两种机制都参与了人类门静脉高压的形成。经典的宏观术语描述了门静脉高压的肝前型、肝内型和肝后型。内脏血流增加是某些肝前型和肝内型门静脉高压的主要原因。肝内门静脉高压已被细分为窦前型、窦型或窦后型。然而，不能将疾病与这种分类一一对应。这些病因中的每一种对肝硬化门静脉压力升高的相对贡献因疾病的病因而异。一种新的导致门静脉高压过程的超微结构分类主要将肝细胞性原因（如肝细胞大小增加）与间质原因（如窦状隙毛细血管化）区分开来。有窗孔的窦状隙内皮细胞在调节肝内阻力以及因此在门静脉高压形成中的作用目前尚不清楚。对前列腺素、白三烯、儿茶酚胺、5-羟色胺等对窦状隙内皮细胞和肝微循环的影响进行全面评估可能为新的治疗途径提供依据。
