Control of hepatic arterial blood flow: independence from liver metabolic activity.
This investigation tested the hypothesis that hepatic arterial blood flow is not dependent on hepatic metabolism, but rather is controlled in a manner that tends to maintain total hepatic blood flow constant. Cats anesthetized with pentobarbital sodium received SKF 525 A or 2,4-dinitrophenol (DNP), respectively, to inhibit or stimulate metabolism. Blood flows and oxygen uptake of the liver and gut were determined by use of a hepatic venous long circuit and noncannulating electromagnetic recording of hepatic arterial blood flow. In both sets of experiments the hepatic arterial blood flow. In both sets of experiments the hepatic artery constricted sufficiently to offset elevated portal venous blood flow, thereby maintaining total hepatic blood flow constant. The reduced hepatic arterial conductance occurred with DNP despite elevated metabolic rate and reduced oxygen in the portal and hepatic veins. Altered gut metabolism correlated with altered vascular conductance in the gut; hepatic arterial conductance changes did not correlate with changes in liver metabolic activity. The data confirmed the hypothesis. It is suggested that for hormonal homeostatis it is essential that total hepatic blood flow be regulated because hepatic clearance is flow dependent.
D000818:Animals; D002415:Cats; D004140:Dinitrophenols / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects; D006499:Hepatic Artery / Q000502:physiology*; D008099:Liver / Q000378:metabolism*; D008102:Liver Circulation / Q000187:drug effects; D010100:Oxygen / Q000097:blood
D004140:Dinitrophenols; D010100:Oxygen