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

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.

Changes in tissue oxygenation of the porcine liver measured by near-infrared spectroscopy

“…[21][22][23] Conversely, the HA blood flow increased significantly in response to PV occlusion, supporting the presence of a hepatic arterial buffer response. 24,25 More importantly, this technique has provided a means of analyzing the relationship between liver parenchymal perfusion, oxygenation, and blood supply. With HA occlusion, there was a reduction in the HbO 2 with a simultaneous increase in Hb that reflects a decrease in the hepatic oxygen supply with a concomitant increase in the fraction of oxygen extracted from blood by the tissue.…”

The role of adenosine in the hyperaemic response of the hepatic artery to portal vein occlusion (the ‘buffer response’)

“…A putative mediator of the response has recently been identified in studies in the cat by Lautt and his colleagues (Lautt et al, 1985), who have concluded that the 'buffer response is mediated entirely by local adenosine concentration' (Lautt & Legare, 1985). They demonstrated that the adenosine receptor antagonist 8-phenyltheophylline totally blocked, and that the adenosine uptake inhibitor dipyridamole potentiated, both the 'buffer response' and the HA vasodilatation induced by injected adenosine.…”

Hepatic arterial buffer response: pathologic evidence in non-cirrhotic human liver with extrahepatic portal vein thrombosis

“…The hepatic arterial flow does not respond to local metabolic or oxygen demands of the liver itself. 9,10,15,16 Ours is the first study to demonstrate histologic changes in hepatic arteries as pathologic evidence for hepatic arterial buffer response in the noncirrhotic human liver. Comparison of arterial measurements of 280 arteries in our series of noncirrhotic portal vein thrombosis patients with 193 arteries in an age-and gender-matched control group demonstrates that there is dilatation of the hepatic arteries as evidenced by a decrease in wall thickness and increase in the percentage of arterial lumen to outer diameter.…”