Hepatic Denervation Induces Supersensitivity to Terbutaline of the Hepatic Arterial System in Conscious Dogs

Abstract

The effects of hepatic denervation on liver blood flow and the influence of the denervation on the hemodynamic response to exogenously administered agents remain equivocal. This study examined the effects of the β2-adrenoceptor agonist, terbutaline, on liver blood flow and how these effects were influenced by surgical hepatic denervation in a conscious canine model. Two weeks after denervation, hepatic arterial flow, portal venous flow, and aortic blood flow were measured during intravenous infusion of terbutaline at 0.1, 0.2, 0.4, and 0.8 μg/kg/min, and responses were compared between the hepatic denervated and sham-operated dogs. Implantable transit-time ultrasonic flowmeter and probes were used. Hepatic arterial flow increased dose-dependently in response to terbutaline in denervated dogs, while it remained unchanged in control dogs except at the highest dose of terbutaline. The increase in hepatic arterial flow of denervated dogs was significantly greater than that of controls at all doses of terbutaline. Aortic blood flow-indexed hepatic arterial flow in response to terbutaline also differed substantially between the two groups. Terbutaline produced a marked dose-dependent increase of portal venous flow similarly in both groups. These results suggest that the β2-adrenoceptor agonist terbutaline should be effective for increasing liver blood flow and could lessen postoperative liver ischemia. We speculate that hepatic denervation induces supersensitivity of the hepatic arterial system to intravenous terbutaline.