Halothane alters the response of isolated airway smooth muscle to carbon dioxide

Rings of canine bronchi were studied in vitro to determine the effects of halothane on the responses of airway smooth muscle to hypercapnia and hypocapnia. Bronchi were first contracted to 50% of maximal active force with acetylcholine (ACh), 5-hydroxytryptamine (5HT), potassium chloride (KCl), or the muscarinic agonist McN-A-343 (McN). The CO₂ concentration of the bathing solution was then changed from 6% to either 1% (hypocapnia) or 10% (hypercapnia). In the absence of halothane, changes in CO₂ concentration had no significant effect on muscles contracted with ACh. With all other contractile agonists, increasing the CO₂ concentration caused bronchial relaxation, while decreasing the CO₂ concentration caused contraction. In the presence of 2 MAC halothane, hypocapnia relaxed bronchi contracted with the muscarinic agonists ACh or McN; the responses to hypocapnia of bronchi contracted with KCl and 5HT were not significantly changed by halothane. Halothane had no effect on the responses of the bronchi to hypercapnia. We conclude that airway smooth muscle contracted with cholinergic agonists relaxes in response to hypocapnia when exposed to 2 MAC halothane; this mechanism may contribute to the depression of hypocapnic bronchoconstriction caused by halothane in vivo.