Regulation of hepatic blood flow: The hepatic arterial buffer response revisited

Abstract

The interest in the liver dates back to ancient times when it was considered to be the seat of life processes. The liver is indeed essential to life, not only due to its complex functions in biosynthesis, metabolism and clearance, but also its dramatic role as the blood volume reservoir. Among parenchymal organs, blood flow to the liver is unique due to the dual supply from the portal vein and the hepatic artery. Knowledge of the mutual communication of both the hepatic artery and the portal vein is essential to understand hepatic physiology and pathophysiology. To distinguish the individual importance of each of these inflows in normal and abnormal states is still a challenging task and the subject of ongoing research. A central mechanism that controls and allows constancy of hepatic blood flow is the hepatic arterial buffer response. The current paper reviews the relevance of this intimate hepatic blood flow regulatory system in health and disease. We exclusively focus on the endogenous interrelationship between the hepatic arterial and portal venous inflow circuits in liver resection and transplantation, as well as inflammatory and chronic liver diseases. We do not consider the hepatic microvascular anatomy, as this has been the subject of another recent review.

Dying to Feel Better

“…Maintenance of global hepatic perfusion by increasing portal contribution results in potentially greater delivery of gut-derived toxins (and proinflammatory factors) under stress. Subsequent falling perfusion limits the ability of the liver to process this load (26). Transient reduction in excretory function can occur without sufficient hepatocellular injury to raise levels of commonly measured liver function tests.…”

Quantitative evaluation of liver cirrhosis using T1 relaxation time with 3 tesla MRI before and after oxygen inhalation

“…Changes to the microenvironment in liver cirrhosis, such as disappearance of the endothelial fenestrae, continuous basement membranes, and extensive depositions of collagen fibers in the Disse's spaces, increase the intrahepatic vascular resistance and decrease the vascular supply to the liver in relation to the cirrhosis severity (23,24). Consequently, portal hypertension occurs in liver cirrhosis with increased vascular resistance (25). As the portal hypertension progresses, the total liver perfusion and the portal venous perfusion in liver cirrhosis progressively decreases with or without increased arterial flow (25,26).…”

“…Consequently, portal hypertension occurs in liver cirrhosis with increased vascular resistance (25). As the portal hypertension progresses, the total liver perfusion and the portal venous perfusion in liver cirrhosis progressively decreases with or without increased arterial flow (25,26). The decreased portal perfusion in liver cirrhosis could be partially compensated by an increase of arterial flow through the hepatic arterial buffer response that may be insufficient to compensate for the decreased portal vein flow up to the normal liver perfusion (27).…”

Arterial and portal venous liver perfusion using selective spin labelling MRI

“…The postprandial arterial perfusion decrease could be explained by the hepatic arterial buffer response (HABR), which is a mechanism for controlling hepatic blood flow. If the portal blood flow increases, the arterial hepatic flow decreases and vice versa [22,23]. A postprandial increase in the portal blood flow is primarily related to a meal-induced splanchnic vasodilation and subsequent flow increase in the superior mesenteric vein [14].…”