Splenic nerve stimulation and epinephrine elevated total resistance and increased small vein pressure primarily through active contraction of the splenic veins in isolated canine spleens.
Canine spleens were isolated and perfused at constant flow with blood from a femoral artery. Perfusion pressure, small vein pressure, tissue cannula pressure, organ weight, and capsular tension were monitored continuously. Splenic nerve stimulation and epinephrine elevated total resistance and increased small vein pressure more than tissue cannula pressure Evidence was provided which demonstrated that the venous pressure increment resulted primarily from active contraction of the splenic veins. Norepinephrine produced equivalent changes in total resistance but was significantly less effective than nerve stimulation and epinephrine, both in raising venous pressure and contracting the splenic capsule. Acetylcholine decreased total resistance, whereas venous pressure was increased by a passive mechanism. The effect of synthetic angiotensin was restricted to contraction of the splenic arterial segments. The highly distensible nature of the spleen was illustrated in experiments where total occlusion of venous flow had only minor effects upon the resistance to arterial inflow. Retrograde perfusion through the splenic vein failed to result in flow out of the splenic artery, indicating that valves or a valvelike mechanism are located at some presinusoidal site along the vascular tree.
Boatman et al. (1964) studied this question. Splenic nerve stimulation and vasoactive agents was evaluated on Vascular responses (perfusion pressure, small vein pressure, tissue cannula pressure, organ weight, capsular tension). Splenic nerve stimulation and epinephrine elevated total resistance and increased small vein pressure primarily through active contraction of the splenic veins in isolated canine spleens.