Richardson P D
Fed Proc. 1982 Apr;41(6):2111-6.
Liver blood flow is determined at normal arterial pressure by 1) the hepatic arterial vascular resistance, 2) the inflow resistance to the preportal vascular beds, 3) the intrahepatic portal venous vascular resistance. Hepatic arterial vascular resistance and therefore blood flow are regulated by relatively weak intrinsic as well as by extrinsic mechanisms. The principal extrinsic mechanisms include the sympathetic vasoconstrictor innervation and epinephrine, whereas the roles of the vasodilator gastrointestinal and pancreatic hormones, and autacoids released from the gastrointestinal tract, remain to be established convincingly. Intrahepatic portal vascular resistance is not significantly controlled by intrinsic mechanisms, and responses to extrinsic mechanisms may be directed principally toward maintenance of portal venous pressure. Two aspects of liver blood flow are discussed in particular detail. First, hormones or drug introduced into one inflow to the liver (e.g., the portal vein) alter the vascular resistance not only of that circuit, but also of the other inflow circuit (hepatic arterial) by a transhepatic mechanism that does not depend on recirculation of the hormone or drug. Second, glucagon, but not other polypeptide vasodilator hormones, prevents hepatic arterial vasoconstriction due to stimuli that include sympathetic nerve activation. This effect occurs at portal or arterial glucagon concentrations close to the pathophysiological range.
在正常动脉压下，肝血流量由以下因素决定：1）肝动脉血管阻力；2）门静脉前血管床的流入阻力；3）肝内门静脉血管阻力。肝动脉血管阻力以及血流量受相对较弱的内在机制和外在机制调节。主要的外在机制包括交感缩血管神经支配和肾上腺素，而血管舒张性胃肠和胰腺激素以及胃肠道释放的自分泌物质的作用仍有待确切证实。肝内门静脉血管阻力不受内在机制的显著控制，对外在机制的反应可能主要是为了维持门静脉压力。肝血流量的两个方面将进行特别详细的讨论。第一，引入肝脏某一血流（如门静脉）的激素或药物，通过一种不依赖于激素或药物再循环的经肝机制，不仅改变该循环的血管阻力，还改变另一血流循环（肝动脉）的血管阻力。第二，胰高血糖素而非其他多肽血管舒张激素，可防止因包括交感神经激活在内的刺激引起的肝动脉血管收缩。这种效应在门静脉或动脉中胰高血糖素浓度接近病理生理范围时出现。
