Some sources say that they are... including the venerable Michels, whose delineations of hepatic arterial supply have generally been considered the standard. Michels even went so far as to say that "each hepatic artery is an end-artery with a selective distribution to a definite area of liver and cannot be sacrificed without resultant necrosis of liver tissue."
The traditional view is that anastomoses between hepatic lobes are observed mainly in the extrahepatic segments (25% of cadaver specimens) and in the liver capsule, as a response to hepatic arterial occlusion (such as with embolization procedures), and that arterial interconnection within the liver parenchyma does not exist.
Others are not so sure, and allow for the possibility of "translobar collateral flow." Their position is that cadaver specimen casts do not demonstrate the tiny connections that in vivo angiography studies do.
In cadaver studies, from which Michels and other earlier anatomists drew their connections, it seems clear that there does not appear to be any interconnection. In an elegant experiment (shown below) Mays and Mays used a resin cast to show no mixing of the arterial supply in the cadaveric human liver.
During angiography, however, evidence of translobar anastomoses is common. In the images below, a
patient referred for coiling of a hepatic pseudoaneurysm after a cholecystectomy was coiled in the pseudoaneurysm and in a proximal branch of the right hepatic artery. On the completion angiogram, the proximal branch at the point of the coils is occluded, but faint filling of some distal branches is evident, compatible with intraparenchymal collateral flow.
Pre-coiling run. A post cholecystectomy pseudoaneurysm is present (red arrow). Distal branches of the right hepatic lobe are opacified (green arrow). |
In a case report from AJR in 1977, embolization of the hepatic artery for blunt trauma was noted to show rapid revascularization, including translobar collateral revascularization, and the authors concluded that "indeed the hepatic artery is not an end artery."
Why the discordance between the cadaver models and the angiography? One source posits neurohormonal alteration of blood flow in the in vivo liver, as a factor allowing for intraparenchymal collateral flow. Another source shows "a widespread bed of fine parenchymal arterioles throughout the liver visible on high-res radiography" and suggest that intrahepatic blood flow, and possibly multifocal hepatocellular carcinoma, may travel via this route. In an article from 1991 in Investigative Radiology, the authors demonstrated tranlobar flow at multiple points (below)
So even though well-written articles in surgical journals have asserted, even into the mid 1990s and beyond, that "the branches of the hepatic artery supplying the liver are essentially end-arteries" (e.g. in the context of careful preservation of arteries in liver transplantation), perhaps this model is incomplete and collateral flow plays a larger role in hepatic perfusion than some have thought.
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1. "Diagnostic Angiography" Kadir S. (1986)
2. Mays II E, Mays E. "Are Hepatic Arteries End Arteries?"
3. Jander HP, Laws HL, Kogutt MS, and Mihas AA. "Emergency Embolization in Blunt Hepatic Trauma" Am J Roentgenol 129:249-252, August 1977
4. Arnold MM, Kreel L, Lo Y, and Law H. "Are the Hepatic Arteries 'End Arteries'?" Investigative Radiology (1991); 26:337-342.
5. Soin AS, Friend PJ, Rasmussen A, et al. "Donor arterial variations in liver transplantation: management and outcome of 527 consecutive grafts" British Journal of Surgery 1996,83, 637-641