Vagally mediated vasodilatation by motor and sensory nerves in the tracheal and bronchial circulation of the pig.

Abstract

A new in vivo model is described in which anaesthetized pigs were used to study vascular responses in the bronchial, upper tracheal and laryngeal circulation upon electrical stimulation of the vagal or superior laryngeal nerves. Vagal or superior laryngeal nerve stimulation increased blood flow in the bronchial artery and the superior laryngeal artery, respectively. After pre-treatment with atropine the vasodilatory response in the bronchial artery upon stimulation was not modified while the increase in blood flow in the superior laryngeal artery was reduced. The ganglionic blocking agent chlorisondamine further reduced the nerve stimulation evoked decrease in vascular resistance in the superior laryngeal artery, but did not influence the response of the bronchial artery. Capsaicin induced a marked increase in blood flow both in the bronchial and superior laryngeal arteries after pre-treatment with atropine, guanethidine and chlorisondamine. After capsaicin tachyphylaxis, the vasodilatation upon nerve stimulation in the bronchial artery and the smaller remaining decrease in vascular resistance in the superior laryngeal artery were strongly reduced. Thus, antidromic stimulation of afferent C fibres may increase blood flow via release of vasodilatory peptides such as tachykinins and calcitonin gene-related peptide. The present findings show that local blood flow in the larynx and upper trachea is regulated by cholinergic and non-cholinergic parasympathetic mechanisms and a small capsaicin sensitive, sensory component. On the other hand, the vagal control of the bronchial circulation seems to exclusively involve capsaicin sensitive sensory nerves.