Nervous control of glycogenolysis and blood flow in arterially and portally perfused liver.

In a recently developed model for the simultaneous perfusion of isolated rat liver via both the hepatic artery (120 mmHg, 20-35% flow) and the portal vein (10 mmHg, 80-65% flow), the arterial and portal nerve plexuses were stimulated (20 V, 2 ms, 2.5-20 Hz for 0.33-5 min) either jointly in the liver hilus or separately at the common hepatic artery and the mesenteric vein, respectively. Stimulation of the arterial plexus alone caused an increase of glucose output, a shift from lactate uptake to output, and a decrease of arterial and, "transhepatically," also of portal flow. Stimulation of the portal plexus alone elicited the same yet clearly smaller metabolic and transhepatic hemodynamic effects. The sum of the metabolic actions of single arterial and portal stimulations but not the sum of the hemodynamic actions was equal to the effects of simultaneous separate stimulations of the hepatic artery and mesenteric vein or joint stimulations in the liver hilus. Half-maximal and maximal effects were reached during 5-min stimulation periods within the physiological range of frequencies, i.e., at 5-6 and 10 Hz for metabolic alterations and at 8 and 20 Hz for hemodynamic changes. At a frequency of 10 Hz, half-maximal and maximal effects were observed with stimulation periods of 0.5 and 1 min for metabolic alterations and with 2 and 5 min for hemodynamic changes. The described model of isolated rat liver perfusion is well suited for the study of the complex metabolic and hemodynamic actions of the arterial and portal nerves, their mutual interactions, and modulations by circulating factors.