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.
The liver receives about 25% of cardiac output. Portal blood accounts for about two-thirds of total flow, and although the liver does not regulate portal flow, it does regulate portal pressure. The hepatic arterial flow is regulated by a unique intrinsic regulatory system, the hepatic arterial buffer response, that is dependent on an adenosine washout mechanism and serves to hold total hepatic blood flow constant. Hepatic arterial flow is not regulated by liver metabolic demands, but rather subserves the hepatic role as a regulator of blood levels of nutrients and hormones by maintaining blood flow and thereby hepatic clearance, as steady as possible. The arterial buffer also plays a role in maintenance of intrahepatic pressures and liver volume. About 30% of hepatic volume is blood (12% of total body blood volume). This total capacitance consists of stressed and unstressed volumes. Stressed volume depends upon intrahepatic pressure and vascular compliance (distensibility). Unstressed volume is the theoretical volume remaining in an organ at zero pressure. Pressures and flows would not be altered if unstressed volume was absent. Active constriction of the capacitance vessels results in transfer of unstressed volume to stressed volume, which maintains or increases venous pressure and venous return. Passive volume changes, secondary to flow changes and thus intrahepatic pressure, are also dramatic in the liver and represent changes in stressed volume. Intrahepatic pressure is virtually equal to portal venous pressure in the normal basal state and is regulated by hepatic venous sphincters. Active hepatic vasoconstriction can result in contraction of these sphincters and also in some presinusoidal constriction. The sphincters appear to be passively distensible, and this characteristic serves to maintain portal and intrahepatic pressures at quite constant levels such that, if inflow decreases, the sphincter resistance increases, and pressure is prevented from a precipitous fall. The intrahepatic pressure maintains sinusoidal patency and allows all sinusoids to be uniformly perfused, even at quite low flows. Fluid and solute exchange between blood and the parenchymal cell is affected by the
In anesthetized cats, reduction of portal flow by occlusion of the superior mesenteric artery results in rapid increase in hepatic arterial (HA) flow that compensates for (buffers) 25.5 +/- 2.7% of the decreased portal flow. The hypothesis tested is that adenosine concentration produced near the HA resistance vessels is regulated by washout into portal vessels in intimate contact with the HA. Reduced portal flow leads to accumulation of adenosine and HA dilation. Several criteria for this hypothesis are met. First, adenosine is a potent dilator of the HA. Second, portal blood has access to HA resistance vessels as shown by a marked dilator effect of adenosine infused into the portal vein; it is therefore possible for adenosine produced locally to diffuse into portal blood. Third, dipyridamole potentiated the dilator response to adenosine as well as potentiating the buffer response from a 23% compensation for reduced portal flow to 34%. Fourth, 1-methyl-3-isobutylxanthine (MIX) antagonized exogenous adenosine and reduced the buffer response from 19% down to 5%. These data strongly support the hypothesis that the hepatic arterial buffer response is mediated by local concentrations of adenosine that are controlled by the rate of washout into portal blood.
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