Bronchial vasodilation evoked by increased lower airway osmolarity in dogs

Abstract

Hyperosmotic saline solutions stimulate lower airway sensory nerves. To determine whether airway hyperosmolarity evokes neurally mediated changes in bronchial artery blood flow (Q˙br), we measured the effect of injection of small volumes (1 ml) of hyperosmotic saline into a right lobar bronchus on Q˙br of anesthetized, artificially ventilated dogs. In 14 dogs, hyperosmotic saline (1,200 and 2,400 mmol/l) increased Q˙br by 58 ± 12 (SE) and 118 ± 12%, respectively, from a baseline of 8 ± 2 ml/min.Q˙br increased within 6–8 s of the injections, peaked at 20 s, and returned to control over 2–3 min. Isosmotic saline had minimal effects. In contrast, hyperosmotic saline decreased flow in an intercostal artery that did not supply the airways. The bronchial vasodilation was decreased by 72 ± 11% after combined blockade of α-adrenoceptors and muscarinic cholinergic receptors and by 66 ± 6% when the cervical vagus nerves were cooled to 0°C. Blockade of H1 and H2 histamine receptors did not reduce the nonvagal response. We conclude that hyperosmolarity of the lower airways evokes bronchial vasodilation by both a centrally mediated reflex that includes cholinergic and adrenergic efferent pathways and by unidentified local mechanisms.