Tracheal mucosal blood flow responses to autonomic agonists

Abstract

In lightly anesthetized adult sheep, we determined tracheal mucosal blood flow (Qtr) by measuring the steady-state uptake of dimethyl ether from a tracheal chamber created by an endotracheal tube provided with two cuffs. Qtr normalized for carotid arterial pressure [Qtr(n)] was determined before and after the exposure of the tracheal mucosa to aerosolized phenylephrine (0.25-2.0 mg), isoproterenol (0.05-0.8 mg), and methacholine (2.5-20 mg). The same doses of methacholine were also administered during the intravenous infusion of vasopressin. The measurements were repeated after intravenous pretreatment with the respective antagonists phentolamine, propranolol, and atropine. Mean +/- SE base-line Qtr(n) was 1.2 +/- 0.1 ml.min-1.mmHg-1.10(2). The autonomic antagonists had no effect on mean Qtr(n). Phenylephrine produced a dose-dependent decrease in mean Qtr(n) (-70% at the highest dose), which was blunted by phentolamine, and isoproterenol produced a dose-dependent increase in mean Qtr(n) (40% at the highest dose), which was blocked by propranolol. Methacholine failed to alter mean Qtr(n) even when Qtr was first decreased by vasopressin. We conclude that in lightly anesthetized adult sheep 1) base-line Qtr(n) is not under adrenergic or cholinergic control, 2) a locally administered alpha-adrenergic agonist decreases and beta-adrenergic agonist increases Qtr(n) via specific receptor activation, and 3) a locally administered cholinergic muscarinic agonist has no effect on Qtr(n).

Inhaled corticosteroids: effects on the airway vasculature in bronchial asthma

“…The sympathetic nervous system provides local control of airway blood flow by releasing norepinephrine, which causes vasoconstriction through activation of a 1 -adrenoreceptors on vascular smooth muscle [98][99][100]. The a 1 -adrenergic responsiveness of airway blood flow has been confirmed in vivo, and additionally shown to be potentiated in asthmatics [94].…”

The bronchial circulation—worth a closer look: A review of the relationship between the bronchial vasculature and airway inflammation

“…Stimulation of alpha receptors causes vasoconstriction and a decrease in flow 56 and beta-adrenergic agonists cause vasodilatation and an increase in flow. 57,58 Whereas the response of both mucosal and total bronchial blood flow to sympathetic stimulation is well documented, the response of the bronchial circulation to parasympathetic stimulation is less clear. The response of the mucosal circulation may differ from that of Q br ; Scuri et al 12 showed that in anesthetized sheep vagal nerve stimulation and intra-arterial acetylcholine (Ach) both increase Q br , whereas the mucosal circulation appears to lack cholinergic muscarinic responsiveness, showing no increase in blood flow following aerosol administration of Ach.…”

Salmeterol Enhances the Inhibitory Activity of Dexamethasone on Allergen-Induced Blood Mononuclear Cell Activation

“…By increasing or decreasing the transcription of genes related to a variety of activities [7,[9][10][11][12], these drugs may downregulate several inflammatory and immune effector cell functions, including proliferation of T lymphocytes [13], release of growth factors [14] and arachidonic acid metabolites by monocytes [15], expression of growth factor receptors [16] and of class II molecules by mononuclear cells [17].…”