Parasympathetic nervous control of tracheal vascular resistance in the dog.

Abstract

1. The dog trachea has a copious subepithelial vasculature supplied at the cranial end by arteries from the superior thyroid artery. The parasympathetic innervation is partly in the superior laryngeal nerves, stimulation of which causes vasodilatation on both sides. 2. Section of these nerves causes a small dilatation, suggesting that there is no significant resting parasympathetic dilator tone. 3. The dilator response to nerve stimulation is about halved when atropine is given, indicating a cholinergic mechanism. 4. The residual vasodilatation on nerve stimulation in the presence of atropine is reduced but not abolished by hexamethonium, suggesting that an antidromic vasodilator pathway can be activated. 5. Stimulation of the nerves increased tracheal mucosal thickness at the same time as vascular resistance decreased. Thus vasodilator mechanisms of parasympathetic origin may contribute to tracheal mucosal swelling and hyperaemia. 6. There is considerable vascular anastomosis between the two sides of the trachea, and possibly also a crossing-over of the parasympathetic innervation.