Molecular mechanisms of systemic vasodilation and hyperdynamic circulatory state of cirrhosis
Molecular mechanisms of systemic vasodilation and hyperdynamic circulatory state of cirrhosis
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DOI：
10.1007/978-1-59259-885-4_4
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发表时间：
2005-01-01
期刊：
影响因子：
--
通讯作者：
Lebrec, D
中科院分区：
文献类型：
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作者：
Moreau, R;Lebrec, D
肝硬变引起的门脉高压与慢性多动症候群有关(1-3)。这种综合征的特征是心输出量增加，动脉压降低，全身血管阻力降低(2，3)。内脏循环也是高度动态的，即供应内脏器官的动脉的血流量增加，血管阻力低(1，4)。全身和内脏的改变是相互关联的：全身血管阻力降低(全身血管扩张)很大程度上是由于内脏动脉阻力降低(内脏血管扩张)(5)。最后，在肝硬变中，存在体内和体外动脉对不同受体依赖和非受体依赖性血管收缩药的低反应性(6-14)。在肝外型门静脉高压症中也会出现高动力综合征，但不如在肝硬变中观察到的那样明显。
Portal hypertension due to cirrhosis is associated with a chronic hyperkinetic syndrome (1–3). This syndrome is characterized by elevated cardiac output, low arterial pressure, and low systemic vascular resistance (2,3). Splanchnic circulation is also hyperdynamic, i.e., blood flow is elevated and vascular resistance is low in arteries that supply splanchnic organs (1,4). Systemic and splanchnic alterations are interrelated: decreased systemic vascular resistance (systemic vasodilation) is largely due to the decrease in splanchnic arterial resistance (splanchnic vasodilation) (5). Finally, in cirrhosis, there is in vivo and ex vivo arterial hyporeactivity to different receptor-dependent and -independent vasoconstrictors (6–14). A hyperkinetic syndrome also occurs in extrahepatic portal hypertension (15), but it is less marked than that observed in cirrhosis.