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肝动脉血流自身调节的机制及作用:肝动脉缓冲反应

Mechanism and role of intrinsic regulation of hepatic arterial blood flow: hepatic arterial buffer response.

作者信息

Lautt W W

出版信息

Am J Physiol. 1985 Nov;249(5 Pt 1):G549-56. doi: 10.1152/ajpgi.1985.249.5.G549.

DOI:10.1152/ajpgi.1985.249.5.G549
PMID:3904482
Abstract

Hepatic parenchymal cell metabolic status does not control the hepatic arterial blood flow. Portal blood flow is a major intrinsic regulator of hepatic arterial tone. Hepatic arterial blood flow changes so as to buffer the impact of portal flow alterations on total hepatic blood flow, thus tending to regulate total hepatic flow at a constant level. This response is called the "hepatic arterial buffer response." The mechanism of the arterial buffer response seems to depend on portal blood flow washing away local concentrations of adenosine (production may be constant) from the area of the arterial resistance site. If portal flow decreases, less adenosine is washed away and the local concentration rises resulting in arterial dilation. Putative roles. Hepatic clearance of many hormones and endogenous compounds is blood flow limited. Constancy of total hepatic blood flow is crucial to homeostasis, and severe changes in the magnitude of flow can rapidly alter plasma concentrations of such compounds. The buffer may also prevent portal flow changes from severely altering intrahepatic blood pressures and liver blood volume. Pathological implications. If the O2 supply-to-demand ratio becomes too low, as in the case of a hypermetabolic liver (chronic alcohol exposure), a state of tissue hypoxia can exist without producing hepatic arterial dilation. Therapeutic implications. Livers show protection and improved recovery from several toxic agents, including alcohol, if the O2 supply-to-demand ratio can be increased. Arterial dilation by means of intra-arterial or intra-portal adenosine may prove useful.

摘要

肝实质细胞的代谢状态并不控制肝动脉血流。门静脉血流是肝动脉张力的主要内在调节因素。肝动脉血流发生变化,以缓冲门静脉血流改变对肝脏总血流量的影响,从而倾向于将肝脏总血流量调节至恒定水平。这种反应被称为“肝动脉缓冲反应”。动脉缓冲反应的机制似乎取决于门静脉血流将动脉阻力部位局部的腺苷浓度(其产生可能恒定)冲走。如果门静脉血流减少,被冲走的腺苷减少,局部浓度升高,导致动脉扩张。假定作用。许多激素和内源性化合物的肝脏清除率受血流限制。肝脏总血流量的恒定对体内平衡至关重要,血流量大小的严重变化可迅速改变此类化合物的血浆浓度。该缓冲反应还可防止门静脉血流变化严重改变肝内血压和肝脏血容量。病理意义。如果氧供需比变得过低,如在肝脏高代谢(长期酒精暴露)的情况下,可能会出现组织缺氧状态而不引起肝动脉扩张。治疗意义。如果能提高氧供需比,肝脏对包括酒精在内的几种毒性物质表现出保护作用且恢复情况会改善。通过动脉内或门静脉内注射腺苷使动脉扩张可能会有帮助。

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