Unilateral cervical vagotomy decreases the magnitude of neurogenic inflammation induced by capsaicin in the ipsilateral bronchial tree of rats

Abstract

Electrical stimulation of a single cervical vagus nerve produces neurogenic inflammation on the stimulated side of the bronchial tree, including the first (main) to the 4th order bronchi. In the contralateral bronchial tree, in contrast, only the proximal part of the main bronchus exhibits inflammatory changes, suggesting that vagal sensory axons present in the bronchi largely originate from the ipsilateral vagus nerve. Intravenous administration of capsaicin can evoke neurogenic inflammation in bilateral bronchial trees. Sensory axons from various sources are thought to be stimulated by this irritant. The extent to which neurogenic inflammation in both bronchial trees might be reduced by unilateral vagotomy is not known. In the present study, we sought to characterize the effect of unilateral cervical vagotomy on capsaicin-induced changes in plasma extravasation and secretory activity of goblet cells in the bronchial trees of both sides. To quantify the magnitude of neurogenic plasma extravasation, Evans blue was used as a tracer dye to measure spectrophotometrically its amount in the bronchial wall. Another tracer dye, Monastral blue, was used to localize the distribution of leaky blood vessels and to measure morphometrically their area density in the whole mounts. To investigate cell and tissue responses of the mucosa, histological methods were employed. After 2 or 4 postoperative weeks, the rats were intravenously administered with a single dose of capsaicin, 150 micrograms/kg. This resulted in different magnitudes of Evans blue extravasation in the bronchi of the two sides in vagotomized rats. Extravasation of Evans blue dye in the bronchial tree ipsilateral to vagotomy was one-half to two-thirds of that of the contralateral bronchial tree.(ABSTRACT TRUNCATED AT 250 WORDS)

Thoracic vagus section distal to the recurrent laryngeal nerve reduces substance

“…This does not inhibit plasma leakage occurring in the contralateral bronchial tree (Huang 1993;Huang et al 1995;Lo and Huang 1997). Intravenously injected SP restores plasma leakage in the bronchi of the vagotomized side (Huang et al 1995).…”

“…Surgical denervation of a single vagal trunk decreases neurogenic plasma leakage induced by capsaicin in the ipsilateral bronchial tree (Huang 1993;Huang et al 1995;Lo and Huang 1997). This does not inhibit plasma leakage occurring in the contralateral bronchial tree (Huang 1993;Huang et al 1995;Lo and Huang 1997).…”

“…Since the SP-IR axons in the tissues are very slender and long using immunohistochemically stained whole mount instead of tissue section is a good choice for a thorough observation of the distribution and quantitation of these axons (Baluk et al 1992;Bowden et al 1996). Surgical degeneration of a single vagal trunk at the midcervical level (Huang 1993;Huang et al 1995) and at the mediastinal level (Lo and Huang 1997) causes a significant decrease in the magnitude of neurogenic inflammation produced by the irritant capsaicin in the ipsilateral bronchial tree of the rat. It is thought that this is due to loss of vagal capsaicin-sensitive SP-containing axons from the mucosa of the affected bronchi.…”

Spontaneous remission of edema and regranulation of goblet cells in rat tracheae after capsaicin-induced acute inflammation

“…After an intravenous injection of capsaicin (McDonald, 1988b;Huang et al 1989;Huang 1993) or substance P (McDonald 1988b;Huang et al 1995), the exudate that leaks out from the venules accumulates largely underneath the mucosal surface epithelium and forms a subepithelial edema. The degree of edema formation and how long it is retained are largely neglected.…”

“…Vagus nerve stimulation causes discharge of mucus granules and is blocked by either atropine or by capsaicin pre-treatment, indicating that both cholinergic nerves ) and capsaicin-sensitive sensory nerves (McDonald 1988a;Huang et al 1989;Tokuyama et al 1990;Kuo et al 1990;Huang 1993;Huang et al 1995) contribute to the control of goblet cell secretion. Capsaicin produces inflammation in the airways by releasing and ultimately depleting substance P from the sensory nerve endings, which acts on the NK-1 receptors.…”