Parasympathetic nervous control of tracheal vascular resistance in the dog.

Abstract

SUMMARY1. 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.

The Effects of Vagal Stimulation on Laryngeal Vascular Resistance and Intraluminal Pressure in the Dog

“…Laitinen et al (1987a) suggested that the superior laryngeal nerve carries predominantly vasodilatory impulses, since electrical stimulation of it always decreases tracheal vascular resistance. This investigator had observed tracheal vasodilation and an increase in tracheal muscle tone, after stimulating the central end of the SLN (vagus intact and RLN intact).…”

“…This response can be blocked by muscarinic agents such as atropine and may be caused by acetylcholine and metacholine (Laitinen et al 1987b). On the other hand, Laitinen et al (1987a) suggested that vasodilatation caused by parasympathetic nerve stimulation in nose and trachea after atropine administration, may be mediated by the release of neuropeptides such as VIP. Recent studies in which the role and distribution of neurotransmitters and neuromodulators are investigated, suggest that NPY, VIP, NOS-1 and CGRP take an important part in the regulation of laryngeal blood flow (Hisa et al 1999 ;Lyon 2000).…”

“…It was shown that the parasympathetic innervation of the dog trachea is partly in the SLN, stimulation of which causes vasodilatation on both sides (Laitinen et al 1987a). On the other hand, stimulation of the central end of a vagus nerve causes tracheal vasoconstriction, systemic hypertension and smooth muscle contraction via impulses came from the cardiac nerves not the pulmonary or abdominal branches of the vagus (Ş ahin et al 1987a).…”

“…Sympathetic nerve stimulation increases their vascular resistance. Although the role of parasympathetic and sympathetic nerves to the laryngeal vascular bed are not well established, the stimulation of superior laryngeal nerve causes nasal and tracheal vasodilatation (Laitinen et al 1987a;Dylewska et al 1993). This response can be blocked by muscarinic agents such as atropine and may be caused by acetylcholine and metacholine (Laitinen et al 1987b).…”

Proceedings of the Physiological Society, 30 June‐ 1 July 1989, Oxford Meeting: Communications

“…Blood flow has been measured recently in the cat tracheal mucosa using a laser Doppler flow-probe (Martling et al 1987). We have compared this method with tracheal artery perfusion pressure at constant flow (Laitinen et al 1987) and blood flow measured using an electromagnetic flow-probe.…”