The role of the splanchnic circulation in the regulation of total intravascular volume during alpha adrenergic receptor stimulation

Abstract

Previous studies have not defined the contribution of the splanchnic circulation to the total intravascular volume change associated with selective alpha adrenergic receptor stimulation. Since the splanchnic circulation is responsible for the total volume changes associated with other types of selective autonomic receptor stimulation, the present study was undertaken to examine the influence of alpha adrenergic receptor stimulation on splanchnic intravascular volume, the hemodynamic mechanism responsible for the splanchnic volume change, and the contribution of the splanchnic volume change to the change in total volume. In 35 anesthetized dogs, blood from the vena cavae was drained into an extracorporeal reservoir and returned to the right atrium at a constant rate so that changes in total intravascular volume could be measured as reciprocal changes in reservoir volume. Phenylephrine infusion (100 micrograms/min) for 20 min in 28 dogs was associated with a decrease in total volume of 64 +/- 17 (SEM) ml (P less than 0.0001). The response was abolished by either alpha adrenergic blockade or evisceration but was not attenuated by beta adrenergic blockade, sinoaortic baroreceptor denervation, ganglionic blockade, or splenectomy. In 5 animals with separate splanchnic perfusion and drainage, total and splanchnic volumes decreased 59 +/- 8 ml (P less than 0.0001) and 317 +/- 20 ml (P less than 0.0001), respectively, while transhepatic vascular resistance increased 17 +/- 4 cm H2O X min/l (P less than 0.0001). These responses were abolished after alpha adrenergic blockade. Thus, splanchnic volume decreases with alpha adrenergic receptor stimulation, despite an increase in hepatic resistance to splanchnic venous outflow. The splanchnic volume decrement is entirely responsible for the total volume decrement.

Influence of α‐adrenergic receptor stimulation on splanchnic intravascular volume in conscious humans

“…This observation may be related to: (1) the different relative contributions of the spleen and li\er to total splanchnic capacit! Finally, although splanchnic venoconstriction caused a decrease in total splanchnic volume despite an increase in the transhepatic resistance to splanchnic venous outflow in the dog (Bell & Rutlen 1986), it is possible that an increase in the transhepatic resistance to splanchnic venous outflow caused an increase in total splanchnic volume despitk splanchnic venoconstriction in the human. In the animal studies, as in the present human studies, phenylephrine was associated with an increase in hepatic volume and decreases in splenic and extrahepatosplenic volume (Bell et ill. 1990).…”

“…Alternatively, it is possible that the use of anaesthetic in the dog contributed to a relatively increased canine splenic capacitance compared to the conscious state. Finally, although splanchnic venoconstriction caused a decrease in total splanchnic volume despite an increase in the transhepatic resistance to splanchnic venous outflow in the dog (Bell & Rutlen 1986), it is possible that an increase in the transhepatic resistance to splanchnic venous outflow caused an increase in total splanchnic volume despitk splanchnic venoconstriction in the human.…”

“…1988al. Numerous studies in animals have demonstrated decreases in splanchnic intravascular volume with selective a-adrenergic receptor stimulation, nonselective adrenergic receptor stimulation, and enhanced sympathetic tone (Brooksby et al 1972, Caldini et al 1974, Karim et al 1976, Karim et al 1978, Rutlen et al 1981, Bell et al 1986, Bell et al 1990). Numerous studies in animals have demonstrated decreases in splanchnic intravascular volume with selective a-adrenergic receptor stimulation, nonselective adrenergic receptor stimulation, and enhanced sympathetic tone (Brooksby et al 1972, Caldini et al 1974, Karim et al 1976, Karim et al 1978, Rutlen et al 1981, Bell et al 1986, Bell et al 1990).…”

“…, Flamm et al 1990. Numerous studies in animals have demonstrated decreases in splanchnic intravascular volume with selective a-adrenergic receptor stimulation, nonselective adrenergic receptor stimulation, and enhanced sympathetic tone (Brooksby et al 1972, Caldini et al 1974, Karim et al 1976, Karim et al 1978, Rutlen et al 1981, Bell et al 1986, Bell et al 1990). Furthermore, studies in our laboratory have demonstrated that the splanchnic volume decrement associated with a-adrenergic receptor stimulation acts to increase cardiac output in animals (Bell et al 1990).…”