EFFECT OF HISTAMINE ON TRACHEAL MUCOSAL PERFUSION, WATER-CONTENT AND AIRWAY SMOOTH-MUSCLE IN SHEEP

We examined the response of tracheal mucosal blood flow normalized for systemic arterial pressure (Qtrn), water content (V(H20)) and luminal dead space (Vtr) to nebulized histamine in intact, lightly anesthetized sheep. Nebulized histamine produced rapid increases in mean Qtrn (+84%) and V(H2O) (+85%), and a decrease in mean Vtr (-17%) (P < 0.05) within 5 min post completion of challenge. Mean Vtr rapidly returned to baseline, while mean Qtrn and V(H2O) remained elevated for 60 and 90 min after challenge, respectively. Pretreatment with chlorpheniramine (H-1-antagonist) blocked the changes in Vtr and V(H2O), and attenuated the increase in Qtrn. Metiamide (H-2-antagonist) pretreatment abolished the increase in Qtrn and blunted the increase in V(H2O), but had no effect on the decrease in Vtr. 2-methylhistamine (H-1-agonist) decreased mean Qtrn and Vtr (P < 0.05) and dimaprit (H-2-agonist) increased mean Qtrn (P < 0.05) without changing Vtr. Neither 2-methylhistamine nor dimaprit significantly altered V(H2O). Atropine blocked histamine induced decreases in Vtr and slightly attenuated the increases in Qtrn and V(H2O). Thus, histamine increased airway smooth muscle tone and mucosal water content principally via H-1 receptors, and mucosal perfusion via H-2 receptors. The airway smooth muscle contraction involved muscarinic pathways.