| Summary: | The hemodynamics of the liver with its dual blood supply is unique. The liver depends entirely on the hepatic artery to regulate total hepatic flow since the portal vein is unable to control inflow to the liver. The existence of stable hepatic blood flow is essential for the maintenance of hepatic functions. The reservoir (capacitance) function, the clearance of many compounds (such as hormones) and the stability of intrahepatic sinusoidal pressure depends on hepatic blood flow. <p>
It has been long observed that the hepatic arterial flow responds in a reciprocal fashion to changes in portal flow in order to maintain total hepatic flow steady, an observation referred to as the hepatic arterial buffer response. On the other hand, the occurrence of changes in hepatic arterial resistance in response to changes in arterial perfusion pressure (i.e. autoregulation) remains controversial. The mechanisms underlying both responses have not been fully elucidated, although a myogenic mechanism has been suggested.<p>
This research study was designed first, to quantitate the hepatic arterial buffer response and the hepatic arterial autoregulation and second, to examine the likely mechanisms governing these responses. An anesthetized cat model with intact liver and intact blood supply was used. The hepatic arterial autoregulation response and the buffer response were induced by the use of a micrometer screw-clamp placed around
the hepatic artery and the superior mesenteric artery. Blood flow in both arteries was measured by electromagnetic flow probes. <p>
The results indicated that the buffer capacity is variable. The buffering efficiency increases with the decrease in portal flow to reach a maximum value of 24% at 60% decrease in portal flow. Although further decreases in portal flow were accompanied by progressive increases in hepatic arterial conductance, the buffering efficiency declined. Our results showed the existence of weak hepatic arterial autoregulation. Both the buffer response and autoregulation were found to be mediated through adenosine. A unified hypothesis has been suggested according to which adenosine is secreted by specialized cells in the space of Mall close to the resistance arterioles of the hepatic artery. This intrinsic dilator can act on the resistance arterioles or be washed away by portal or hepatic arterial flow. Reduction in either flow would result in accumulation of adenosine resulting in vasodilation of the hepatic artery. An increase in either flow would result in vasoconstriction. Our data support the dilator washout theory.
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