Significance of Catecholamine-Induced Ganglionic Blockade and of Reflex Inhibition of Adrenergic Discharge at a Peripheral Locus as Mechanisms Producing Reflex Vasodilatation

Abstract

An analysis has been made of the various factors which contribute to the vasodilatation observed in the innervated perfused hindlimb when catecholamines are injected intravenously. Bilateral transection of the lumbar sympathetic chains abolishes all dilatation in some animals and greatly reduces dilatations in all animals. When the sympathetic tone lost by chain transection is restored by preganglionic stimulation, the residual hindlimb dilatation still present after chain section is often increased, and a component of dilatation appears de novo in the hindlimb of many animals. This dilatation was blocked by spinal anesthesia. It is concluded that: (1) the peripheral dilatation produced in the hindlimb of the dog by intravenously administered catecholamines is almost entirely reflex in origin; (2) blockade of ganglionic transmission by intravenously injected adrenergic amines does not contribute significantly to the production of reflex dilatation; (3) the residual dilatation remaining after transection of the sympathetic chains is also reflex in origin because it is blocked by spinal anesthesia; (4) the hindlimb vasodilatation which appears de novo during stimulation of the sympathetic chain is also abolished by spinal anesthesia and is apparently due to inhibition of adrenergic discharge at a peripheral locus; (5) in the pentobarbital anesthetized dog, little, if any, of the hindlimb dilatation resulting from the intravenous injection of epinephrine is due to predominant activation of beta receptors.