β-adrenergic regulation of total systemic intravascular volume in the dog

While it is known that β-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 cardiopulmonary 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 μg/min) or norepinephrine infusion (30 μg/min). At central venous pressures of 3, 8, and 13 cm H₂O, 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 H₂Oxmin/l (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 H₂Oxmin/l (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 2 other animals. Decreases in hepatic resistance, splanchnic volume, and total volume were abolished after propranolol. Thus, β-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.