BACKGROUND: A rapid increase in isoflurane concentration induces tachycardia and hypertension and increases plasma catecholamine concentration. The current study examined the effects of the rate of increase in inhaled isoflurane concentration on the circulatory responses. METHODS: Unpremedicated sixty three ASA physical status 1 patients, aged 20-40 years, scheduled for elective surgery under general anesthesia were randomly allocated into one of three groups. In each group, the inspired concentration of isoflurane via mask was increased up to 5 vol% at the rate different from other groups. The inspired concentration of isoflurane via mask was increased to 5.0 vol% abruptly (group 1), for 100 seconds (group 2), or 200 seconds (group 3). The target was to produce an end-tidal concentration of isoflurane (ETisof) of 2.6 vol% which was maintained until the end of the study by adjusting the vaporizer setting, when necessary. Heart rate (HR), mean arterial pressure (MAP), ETisof, end-tidal concentration of carbon dioxide, and peripheral oxygen saturation were measured at baseline and every 30 seconds for 5 minutes after inhalation of isoflurane and for 2 minutes after intubation. RESULTS: HR and MAP were significantly increased in all three groups compared with baseline, but significant differences in maximum values were not observed in three groups. There were significant differences among the groups in time from the onset of isoflurane inhalation to the maximal effect on HR and MAP. However, there were no significant differences among the groups of the ETisof at the maximal HR and MAP were seen. CONCLUSIONS: The high concentration of isoflurane transiently increase HR and MAP during inhaled anesthesia induction. However, the rate of increase in inhaled isoflurane concentration does not affect the circulatory responses.