Kim Moon Young, Baik Soon Koo
Department of Internal Medicine, Institute of Basic Medical Science, Yonsei University Wonju College of Medicine, Wonju, Korea.
Korean J Gastroenterol. 2009 Sep;54(3):143-8. doi: 10.4166/kjg.2009.54.3.143.
Hyperdynamic circulation in patients with liver cirrhosis is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure and currently focused on understanding the pathogenesis because of possibility of developing novel treatment modality. Basically, these hemodynamic alternations arise from portal hypertension. Portosystemic collaterals develop to counterbalance the increased intrahepatic vascular resistance to portal blood flow and induce an increase in venous return to heart. Increased shear stress in vascular endothelial cell related high blood flow by portosystemic shunting contributes to this upregulation of eNOS resulting in NO overproduction. Additionally, bypassing through portosystemic collaterals and escaping degradation of over-produced circulating vasodilators in the diseased liver can promote the peripheral arterial vasodilation. Vasodilation of the systemic and splanchnic circulations lead to a reduced systemic vascular resistance, and increased cardiac output and splanchnic blood flow. Furthermore, neurohumoral vasoconstrictive systems including systemic nervous system, rennin angiotensin aldosterone system, and vasopressin are intensively activated secondary to vasodilation. However, hyperdynamic circulation would be more aggravated by the activated vasoconstrictive systems. With the progression of the cirrhotic process, hyperdynamic alternations can be more profound due to hyporesponsiveness to vasoconstrictors and increased shunt formation in conjunction with autonomic neuropathy. Eventually, splanchnic arterial vasodilation results in an increase portal venous inflow, maintaining the elevated portal venous pressure. Hyperdynamic circulation is intimately involved in portal hypertension with liver cirrhosis, therefore it is reasonable to have an interest in complete understanding of the pathogenesis of hyperdynamic circulation to develop novel treatment modality.
肝硬化患者的高动力循环特征为心输出量和心率增加，全身血管阻力降低，动脉血压偏低，目前由于可能开发新的治疗方式而专注于了解其发病机制。基本上，这些血流动力学改变源于门静脉高压。门体侧支循环形成以平衡肝内门静脉血流阻力增加，并导致静脉回心血量增加。门体分流导致血管内皮细胞处高血流相关的剪切应力增加，这有助于内皮型一氧化氮合酶上调，导致一氧化氮过度产生。此外，通过门体侧支循环的分流以及患病肝脏中过度产生的循环血管扩张剂逃脱降解可促进外周动脉血管扩张。全身和内脏循环的血管扩张导致全身血管阻力降低，心输出量和内脏血流量增加。此外，包括交感神经系统、肾素 - 血管紧张素 - 醛固酮系统和血管加压素在内的神经体液血管收缩系统在血管扩张继发下被强烈激活。然而，激活的血管收缩系统会使高动力循环更加严重。随着肝硬化进程的进展，由于对血管收缩剂反应性降低以及与自主神经病变相关的分流形成增加，高动力改变可能会更严重。最终，内脏动脉血管扩张导致门静脉流入增加，维持门静脉压力升高。高动力循环与肝硬化门静脉高压密切相关，因此有必要深入了解高动力循环的发病机制以开发新的治疗方式。
