Hepatic arteriolo-portal venular shunting guarantees maintenance of nutritional microvascular supply in hepatic arterial buffer response of rat livers

1. To elucidate the hepatic microvascular response upon the hepatic arteria l buffer response (HABR), we analysed blood flow (ultrasonic flowprobes) of the hepatic artery (HA) and portal vein (PV), microcirculation (intravital microscopy), and tissue oxygenation (polarography) in anaesthetized Spragu e-Dawley rats and re-evaluated the role of adenosine in mediating the HABR by using 8-phenyltheophylline as a competitive antagonist. 2. Upon restriction of PV blood flow to 11 +/- 3% of baseline values, HA bl ood flow increased by a factor of 1.77 (P < 0.05), thus confirming HABR. St rikingly, red blood cell velocity and volumetric blood flow in terminal hep atic arterioles (THAs) did not increase but were even found to be slightly decreased, by 8 and 13%, respectively. In contrast, red blood cell velocity and volumetric blood flow in terminal portal venules (TPVs) decreased to o nly 66% (P < 0.05), indicating upstream hepatic arteriolo-portal venular sh unting. As a consequence, red blood cell velocity and volumetric blood flow in sinusoids were found to be reduced to only 66-68% compared with baselin e (P < 0.05). Diameters of neither of those microvessels changed, thus excl uding THA-, TPV-, and sinusoid-associated mechanisms of vasomotor control i n HABR. 3. Tissue P-O2 and hepatocellular NADH fluorescence remained unchanged, ind icating HABR-mediated maintenance of adequate oxygen delivery, despite the marked reduction of total liver blood flow. Further, hepatic arteriolo-port al venular shunting guaranteed homogeneity of nutritive blood flow upon HAB R, as given by an unchanged intra-acinar coefficient of variance of sinusoi dal perfusion. 4. Pretreatment of animals with the adenosine antagonist 8-phenyltheophylli ne completely blocked the hepatic arterial buffer response with the consequ ence of decreased tissue oxygenation and increased heterogeneity of sinusoi dal perfusion. 5. In conclusion, hepatic microhaemodynamics, in particular unchanged diame ters of THAs, TPVs and sinusoids, during HABR indicate that reduction in re sistance to HA flow is located upstream and functions via hepatic arteriolo -portal venular shunts resulting in equal distribution of microvascular blo od flow and oxygen delivery under conditions of restricted PV blood supply.