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1995年汽巴-嘉基奖讲座。肝血流的内在调节。

The 1995 Ciba-Geigy Award Lecture. Intrinsic regulation of hepatic blood flow.

作者信息

Lautt W W

机构信息

Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.

出版信息

Can J Physiol Pharmacol. 1996 Mar;74(3):223-33.

PMID:8773400
Abstract

Intrinsic regulation of hepatic blood flow is mediated only through the hepatic artery because the liver is not able to directly regulate portal vein blood flow. Hepatic metabolic activity does not affect hepatic artery flow. Although the hepatic artery is affected by sympathetic nerves and blood-borne agents, the intrinsic regulation of the hepatic artery can be demonstrated if these factors are controlled. The primary intrinsic regulator of the hepatic artery is the hepatic arterial buffer response, which is the inverse response of the hepatic artery to changes in portal vein flow. The hepatic arterial buffer response is sufficiently powerful that doubling portal vein flow leads to maximal constriction in the hepatic artery, while low portal vein flow can result in maximal dilation. The mechanism of the hepatic arterial buffer response is based on adenosine washout, whereby adenosine is produced at a constant rate, independent of oxygen supply or demand, and secreted into a small fluid compartment that surrounds the hepatic arterial resistance vessels. If portal vein flow decreases, less adenosine is washed away into the portal blood and the accumulated adenosine leads to hepatic arterial dilation. Similarly, hepatic arterial autoregulation operates by the same mechanism, whereby a decrease in arterial pressure leads to a decrease in hepatic arterial flow, thus resulting in less adenosine washout into the hepatic artery blood. The accumulated adenosine leads to hepatic artery dilation. These intrinsic regulatory mechanisms tend to maintain total hepatic blood flow at a constant level, thus stabilizing hepatic clearance of hormones, venous return, and cardiac output.

摘要

肝血流的自身调节仅通过肝动脉介导,因为肝脏无法直接调节门静脉血流。肝脏代谢活动不影响肝动脉血流。尽管肝动脉受交感神经和血源性激素的影响,但如果控制这些因素,仍可证明肝动脉的自身调节。肝动脉的主要自身调节机制是肝动脉缓冲反应,即肝动脉对门静脉血流变化的反向反应。肝动脉缓冲反应非常强大,门静脉血流加倍会导致肝动脉最大程度收缩,而门静脉血流较低时则会导致最大程度扩张。肝动脉缓冲反应的机制基于腺苷清除,即腺苷以恒定速率产生,与氧供应或需求无关,并分泌到围绕肝动脉阻力血管的小液腔中。如果门静脉血流减少,进入门静脉血中的腺苷被冲走的量减少,积累的腺苷会导致肝动脉扩张。同样,肝动脉自身调节也通过相同机制起作用,即动脉压降低会导致肝动脉血流减少,从而使进入肝动脉血中的腺苷清除减少。积累的腺苷会导致肝动脉扩张。这些自身调节机制倾向于将肝脏总血流量维持在恒定水平,从而稳定肝脏对激素的清除、静脉回流和心输出量。

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