Autonomic stimulation and blockade on canine splenic inflow, outflow and weight

¹ Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest College, Winston-Salem, North Carolina

Blood flow (autoperfusion-electromagnetic meters), pressures and splenic weight (strain gauges) were recorded in barbitalized dogs. Splenic nerve stimulation and epinephrine decreased inflow, increased outflow and pressure and diminished splenic weight; during recovery inflow exceeded outflow, and splenic weight returned to control. Progressively increasing adrenergic blockade partially reversed the inflow reduction (vasoconstriction) but only decreased the outflow surge and weight reduction. Cholinergic substances increased inflow, outflow and splenic weight; atropine abolished these without significant effect on adrenergic or splenic nerve responses. No reactive vasodilation followed interruption of inflow. Conclusions: a) metabolic dilator receptors are absent; b) afferent arterioles possess innervated adrenergic constrictor receptors and noninnervated ß adrenergic and cholinergic dilator receptors; c) an innervated ‘emptying mechanism’ exists which may: 1) involve efferent venular relaxation and/or contraction of smooth muscle in the capsule or substance of the spleen, 2) have neither receptors (arterenol is minimally effective and the response is resistant to adrenergic blockage) nor ß receptors (isoproterenol is ineffective) and 3) have epinephrine as its neuromediator.