Blendis L, Wong F
Institute of Gastroenterology, Sourasky Tel Aviv Medical Center, 6 Weizman Street, Tel Aviv 64239, Israel.
Pharmacol Ther. 2001 Mar;89(3):221-31. doi: 10.1016/s0163-7258(01)00124-3.
The hyperdynamic circulation begins in the portal venous bed as a consequence of portal hypertension due to the increased resistance to flow from altered hepatic vascular morphology of chronic liver disease. Dilatation of the portal vein is associated with increased blood flow, as well as the opening up or formation of veno-venous shunts and splenomegaly. At the same time, portal hypertension leads to subclinical sodium retention resulting in expansion of all body fluid compartments, including the systemic and central blood volumes. This blood volume expansion is associated with vasorelaxation, as manifested by suppression of the renin--angiotensin--aldosterone system, initially only when the patient is in the supine position. Acute volume depletion in such patients results in normalisation of the hyperdynamic circulation, whilst acute volume expansion results in exaggerated natriuresis. As liver disease progresses and liver function deteriorates, the systemic hyperdynamic circulation becomes more manifest with activation of the renin--angiotensin--aldosterone system. The presence of vasodilatation in the presence of highly elevated levels of circulating vasoconstrictors may be explained by vascular hyporesponsiveness due to increased levels of vasodilators such as nitric oxide, as well as the development of an autonomic neuropathy. However, vasodilatation is not generalised, but confined to certain vascular beds, such as the splanchnic and pulmonary beds. Even here, the status may change with the natural history of the disease, since even portal blood flow may decrease and become reversed with advanced disease. The failure of these changes to reverse following liver transplantation may be due to remodelling and angiogenesis.
由于慢性肝病导致肝血管形态改变，血流阻力增加，进而引起门静脉高压，高动力循环始于门静脉床。门静脉扩张与血流量增加、静脉-静脉分流的开放或形成以及脾肿大有关。同时，门静脉高压导致亚临床钠潴留，致使包括全身和中心血容量在内的所有体液腔室扩张。这种血容量扩张与血管舒张有关，最初仅在患者仰卧位时表现为肾素-血管紧张素-醛固酮系统受抑制。此类患者急性容量耗竭会使高动力循环恢复正常，而急性容量扩张则会导致尿钠排泄增加。随着肝病进展和肝功能恶化，肾素-血管紧张素-醛固酮系统激活，全身高动力循环变得更加明显。在循环血管收缩剂水平大幅升高的情况下出现血管舒张，可能是由于一氧化氮等血管舒张剂水平升高以及自主神经病变导致血管反应性降低所致。然而，血管舒张并非全身性的，而是局限于某些血管床，如内脏和肺血管床。即便在此处，随着疾病自然进程，情况也可能发生变化，因为在疾病晚期，甚至门静脉血流也可能减少并出现逆流。肝移植后这些变化未能逆转可能是由于重塑和血管生成。
