EFFECTS OF HALOTHANE, PROPOFOL, AND THIOPENTAL ON PERIPHERAL AIRWAY REACTIVITY

Background. General anesthetics modify airway responsiveness by severa l mechanisms, including direct effects on airway smooth muscle and red uctions in neural reflex activity. Halothane has been shown to reduce responsiveness through both of these mechanisms. The airway effects of barbiturates are controversial, and the effects of propofol are unkno wn. Methods: To compare the direct effects of halothane, thiopental, a nd propofol in vivo, canine peripheral airways were constricted with t wo stimuli, histamine and hypocapnia, which are thought to directly co ntract smooth muscle. The authors then investigated the role of ATP-se nsitive potassium (K(ATP)) channels as a mechanism for attenuating the se responses. Basenji-Greyhound (BG) dogs were anesthetized with eithe r halothane (1.5 MAC), thiopental (7.5 mg.kg-1 . min-1 intravenously) plus fentanyl (25 mug intravenously every 20-30 min), or propofol (0.6 mg . kg-1 . min-1 intravenously). A wedged bronchoscope technique was used to measure peripheral airway resistance (R(p)). After a stable b aseline was obtained, dose-response curves to histamine (50, 100, or 2 00 mug intravenous bolus) or hypocapnia (0% CO2 for 2 min with 100, 20 0, or 400 ml/min collateral flow) were constructed. On separate occasi ons, the same sublobar segments were pretreated with glibenclamide (2 mg/ml aerosol), a K(ATP) channel blocker, and dose-response curves to hypocapnia were repeated. Results. Dose-response curves to histamine w ere similar during all three anesthetics. Halothane decreased airway r esponsiveness to hypocapnia, compared with either thiopental or propof ol (P < 0.05). Pretreatment with glibenclamide abolished the effect of halothane on hypocapnia-induced airway constriction. Conclusions: The se results indicate that propofol afforded no benefit over thiopental or halothane in reducing peripheral airway responsiveness. Furthermore , the beneficial effects of halothane in reducing responsiveness to hy pocapnia appear to be mediated by the opening of K(ATP) channels.