Catecholamine-induced Changes in the Splanchnic Circulation Affecting Systemic Hemodynamics

Abstract

Nearly 25% of the total blood volume in humans resides within the splanchnic venous vasculature. In healthy normovolemic adults, sympathoadrenal stimulation can almost instantaneously transfuse approximately 2 units of whole blood from the splanchnic to the systemic circulation (table 2). α-Adrenoceptor stimulation actively expels blood from splanchnic capacitance vessels, producing a rapid increase in venous return. This volume mobilization occurs because of active venoconstriction as well as passive elastic recoil of the splanchnic veins secondary to decreased arterial inflow. The initial increase in venous return may be counteracted by other α-adrenergic effects, such as an increase in hepatic venous resistance (which impedes expulsion of blood from the splanchnic to the central circulation) and a significant decrease in splanchnic arterial flow (which pharmacologically removes a portion of the systemic circulation). The degree to which an α-adrenergic agonist affects venous return and cardiac output is therefore dependent on many factors, including baseline myocardial contractility, blood volume, and sympathetic tone. Pure β-adrenergic agonists (e.g., isoproterenol) augment cardiac output primarily by increasing venous return, which results from increases in splanchnic blood flow due to lowered resistances in splanchnic arterial vessels and hepatic veins. In general, a drug that stimulates both α- and β-adrenergic receptors would be expected to more effectively maintain systemic hemodynamics than one that activates either α- or β-adrenergic receptors. When simultaneously stimulated, α- and β-adrenergic receptors act in concert to maximally shift blood from the splanchnic vasculature into the systemic circulation by producing vasoconstriction, decreasing splanchnic vascular capacitance, and decreasing (or minimizing the increase in) intrahepatic vascular resistance.