1. In chloralose-anaesthetized, artificially ventilated dogs, the splenic p
edicle was tied and the carotid sinuses were vascularly isolated and perfus
ed at controlled pressures. In Series 1 experiments, the hepatosplanchnic c
irculation was perfused through the abdominal aorta with a tie on the aorta
separating it from the caudal circulation, which was perfused through the
femoral arteries. The two circulations were drained from cannulae in the in
ferior vena cava and the femoral veins, with a,tie on the inferior vena cav
a separating the two. In Series 2, the splanchnic circulation drained from
the portal vein. In both series, inflows and outflows were measured and int
egrated to derive volume changes. Capacitance responses were assessed durin
g constant flow, and capacitance plus passive responses were obtained durin
g constant pressure perfusion.
2. In Series 1, an increase in carotid sinus pressure (from 8 to 26 kPa) du
ring constant flow and constant pressure perfusion increased hepatosplanchn
ic volume by 2.5 and 5.7 ml (kg body weight)(-1), respectively. The volume
of the subdiaphragmatic circulation did not increase during constant flow,
but during constant pressure it increased by 2.0 mi (kg body weight)(-1).
3. In Series 2, increasing carotid pressure during constant flow and consta
nt pressure increased the volume of the splanchnic circulation by 0.5 and 4
.2 mi (kg body weight)(-1), respectively.
4. These results confirm that carotid baroreceptor stimulation causes large
r volume changes during constant pressure perfusion than during constant fl
ow perfusion. Also, the active capacitance change in the splanchnic circula
tion is small in relation to the passive response. We propose that in dogs
(following splenic ligation), the major active capacitance control is from
the liver. However, large passive changes in splanchnic volume occur due to
changes in flow.