Volatile anesthetics are effective at preventing and reversing bronchospasm, but their effects on baseline airway tone are controversial. While tantalum bronchography has been used in the past to measure one-dimensional airway diameter changes, this method has inherent problems associated with the irritant effects of tantalum. Until recently, no other direct noninvasive in vivo method to assess airway caliber was available. The present investigation assesses the effects of the inhalation anesthetic halothane on individual unstimulated airways in vivo. Ten studies were performed in seven dogs. All dogs were initially anesthetized with 15 mg/kg thiopental followed by a 10-mg.kg-1 x h-1 maintenance dose. Following tracheal intubation the lungs were mechanically ventilated (15 ml/kg, 15 beats/min). The dogs subsequently received increasing doses of halothane (range 0.5-1.5%). On a separate day, the dogs were pretreated with atropine (0.2 mg/kg) and the study was repeated. Fifty sequential high-resolution computed tomography scans were obtained using a 1-s scan time, 137 kVp, 220 mA, 2-mm slice thickness, and 1-mm table feed. Airway areas ranging in size from 3 to 22 mm in diameter were measured and analyzed by one way analysis of variance and Bonferroni pair-wise comparisons of means. Halothane in concentrations of 0.5%, 1.0%, and 1.5% showed significant dose-dependent dilation of the airways (percent increase from control) that averaged 90 +/- 19% (mean +/- SEM), 128 +/- 20%, and 182 +/- 27%, respectively (P = .017). Atropine pretreatment alone significantly dilated the airways to 151 +/- 25% (P = .002) of their baseline value. Halothane caused no further airway dilation in atropine pretreated dogs. Halothane dilates baseline airways by blocking baseline vagal tone. Since baseline airway tone, airway wall thickness, and initial airway diameter are major determinants of airway reactivity, the observed dilation by halothane may be one of the mechanisms by which inhalational anesthetics decrease airway reactivity.