beta-Adrenergic regulation of total systemic intravascular volume in the dog.

While it is known that /?-adrenergic receptor stimulation is associated with an increase in venous return, the mechanism by which this increase is mediated has not been well defined. A total of 55 dogs were anesthetized, placed on cardiopubnonary bypass, and perfused at a constant rate. In 23 of these animals, changes in total systemic intravascular volume were measured as reciprocal changes in extracorporeal reservoir volume during isoproterenol (6 /ig/min) or norepinephrine infusion (30 pg/ min). At central venous pressures of 3, 8, and 13 cm H 2 O, isoproterenol was associated with decreases in intravascular volume of 70 20 (standard error of the mean) (P < 0.02), 50 20 (P < 0.05), and 20 30 (NS) ml, respectively, and norepinephrine was associated with decreases of 300 60 (P < 0.001), 230 30 (P< 0.001), and 190 40 (P< 0.001) ml, respectively. The splanchnic vasculature was perfused selectively at a constant rate and drained separately in another 18 animals. In these dogs, an isoproterenol-associated decrease in splanchnic volume occurred concomitantly with a decrease in postsinusoidal hepatic vascular resistance from 38 5 to 18 3 cm H 2 Omin/liter (P< 0.001). A norepinephrine-associated decrease in splanchnic volume occurred simultaneously with a decrease in hepatic vascular resistance from 33 6 to 18 2 cm H 2 Omin/liter (P < 0.001). The decreases in total intravascular volume obtained with either isoproterenol or norepinephrine were abolished after the splanchnic vasculature had been removed in two other animals. Decreases in hepatic resistance, splanchnic volume, and total volume were abolished after propranolol. Thus, yS-adrenergic receptor stimulation with either isoproterenol or norepinephrine is associated with a decrease in transhepatic vascular resistance and subsequent decreases in splanchnic and total systemic intravascular volume.