The liver blood supply portrays one of the most sophisticated archetypes of circulation. Despite its weight (representing only 2.5% of body weight), the liver receives 25% of the cardiac output, allowing the hepatic parenchyma to be the most richly perfused of any organ. The anatomical distinctiveness of the double afferent blood supply is established between the hepatic artery and the portal vein, ensuring a total blood flow of 100 to 130 mL/min per 100 g of liver. Approximately 20 to 25% of the blood perfusing the liver is well oxygenated, and is provided by the hepatic artery. In addition to hepatic parenchymal cells, the hepatic artery provides the exclusive blood supply to the intrahepatic bile ducts. The portal vein, formed by the confluence of the splenic vein, mesenteric veins, gastric veins, and pancreatic vein, supplies around 75 to 80% of the afferent blood, which is partially deoxygenated.[1] [2] Mixing of arterial and portal blood occurs in the sinusoids, an exclusive, dynamic microvascular structure that serves as the principal site of exchange between the blood and the perisinusoidal space.[3] The hepatic veins (typically three—right, middle, and left) drain the blood from those locations into the inferior vena cava.

While the hepatic flow control mechanism has been studied extensively, some features, in particular the relationship between hepatic arterial and venous circulation, remain unclear.[4] As with other organs, the liver also strives for constant blood flow. This modulation, however, is not dependent on extrinsic innervation or vasoactive agents, but rather on a pressure-dependent autoregulation mechanism. Due to this, if the portal vein flow changes, the hepatic arterial flow is shifted in the opposite direction. This biological behavior is known as hepatic arterial buffer response (HABR).[5]

Alternate hypotheses to pressure-dependent autoregulation have been considered to account for this phenomenon, including neural and myogenic mechanisms.[1] [4] The neural mechanism has been rebuffed by observing the HABR even in denervated livers. Likewise, the myogenic mechanism, which proposed that a change in portal pressure would be somehow sensed by the hepatic artery, was excluded since changes in portal pressure are quite slight despite even major changes in portal flow.[6] [7] The most accepted theory for HABR is the adenosine washout hypothesis. In line with this theory, increased portal flow leads to a reduction of adenosine concentration and hepatic arterial constriction. Oppositely, when the portal blood flow is reduced, the amount of adenosine that accumulates in the Mall space will increase, as it will not be washed away by portal flow, leading to dilation of the hepatic artery (adenosine is a powerful vasodilator), and this effect has been studied by several investigators.[8] [9] [10] [11] As demonstrated by Lautt et al, dipyridamole, which inhibits the nucleoside transporter responsible for the cellular uptake of adenosine, potentiates the dilator response to adenosine as well as potentiating the buffer response from a 23% compensation for reduced portal flow to 34%.[8] The dilator effect of adenosine is less in the portal vein, and has approximately one-half to one-third the effect of the same dose infused directly into the hepatic artery.[1]

Article published online:
04 May 2023

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