The function of the hepatic artery has been extensively studied in animals (1-5). Great differences have been found from one species to another (6, 7), and our knowledge of the significance of the arterial blood supply to the human liver is limited mainly to observations of the late effect of occlusion of the hepatic artery (8) or of the portal vein (9, 10). As these events are followed by compensatory changes in the hepatic circulation (11,12), no definite conclusions regarding the physiological role of the hepatic artery can be made on this basis. It might be expected that acute, transitory interruption of the blood flow through the hepatic artery minimizes this compensation and thus gives a clearer picture of the function of the artery.
METHODSThe eight patients of this study were premedicated in the ward with morphine and atropine, and transferred to the catheterization room, where a Cournand catheter was introduced via a left antecubital vein into one of the major right hepatic veins, and a small polyethylene tube was inserted percutaneously into the left femoral artery. The patient was then taken to the operating theater, where anesthesia (barbiturate, muscle relaxant, and nitrous oxide-oxygen with intubation) was given. Soon afterward an intravenous infusion of sulfobromophthalein (BSP) was started, after a priming dose of 150 mg. The time of this injection was used as reference time.Immediately after the opening of the peritoneal cavity the hepatic artery was isolated, a clamp was loosely placed around the hepatic artery proper distal to the gastroduodenal and right gastric branches, and a catheter was introduced into the portal vein through a vein in the mesocolon. After these procedures the field was covered, and no further intraperitoneal manipulations were performed during the study. When the determinations of the control period were completed, the clamp on the hepatic artery was closed, and a second series of determinations was performed during the clamping period which lasted on the average 24 minutes.All three catheters were connected to stopcocks outside the field and regularly flushed with saline containing heparin. Blood samples were drawn simultaneously from the catheters into heparinized syringes after the first 10 ml had been discarded.In each period five samples (average) were drawn for the determination of BSP concentrations by method I of Winkler, Tygstrup and Munkner (13). In the middle of each period or, in five cases, twice during the clamping period, blood was drawn for the determination of oxygen tension [polarographic method, (14)], oxygen saturation (reflectometry), hemoglobin concentration, hematocrit, serum glutamic-oxalacetic acid transaminase, serum glutamic-pyruvic acid transaminase, lactic acid dehydrogenase, carbon dioxide tension, and pH (15). The oxygen content was calculated from the saturation and the oxygen capacity (derived from the hemoglobin concentration), and the oxygen tension. An average of 400 ml of blood was drawn for these determinations, and the loss was repl...