Korean J Anesthesiol intubation and 1, 2 and 3 minutes after intubation. In Group FN, the MAP was increased just after endotracheal intubation compared to the baseline MAP (98.4 ± 17.3 mmHg vs 86.6 ± 10.0 mmHg, respectively) (Fig. 2A, P < 0.05). The heart rate in Group FN just after endotracheal intubation was higher than the baseline heart rate (88.6 ± 22.8 bpm vs 77.1 ± 14.8 bpm, respectively). It was significantly increased at 1 and 2 minutes after intubation (Fig. 2B, P < 0.05). In Group FS, the heart rate just after intubation was increased higher than that of baseline (88.9 ± 10.8 bpm vs 72.4 ± 3.9 bpm, respectively), and it was significantly increased at 1, 2 and 3 minutes after intubation (Fig. 2B, P < 0.05). But there was no difference in the heart rate between Groups FN and FS (Fig. 2B). Discussion Endotracheal intubation is a commonly used, necessary maneuver for securing the airway when inducing general anesthesia. However, endotracheal intubation causes the stimulation of the sympathetic nervous system, which increases the plasma catecholamine level and this can cause an elevated blood pressure and tachycardia [9]. Most myocardial ischemia that occurs during anesthesia is related to endotracheal intubation and especially to tachycardia [10]. So it is important to prevent hemodynamic changes during anesthetic induction. To minimize such cardiovascular responses, the use of opioids, local anesthetics, inhalational anesthetics, beta adrenergic blockers, calcium channel blockers and other cardiovascular drugs has been shown to be effective [11]. Among them, opioids have been the most widely used drugs. Fentanyl blocks the sympathetic nervous responses during anesthetic induction. The amount of fentanyl used for endotracheal intubation with Sung, et al. using a laryngoscope is known to be directly proportional to the ability to suppress the cardiovascular response, so fentanyl has often been used [12], yet remifentanil has recently become more widely used. There have been many studies on what the appropriate dosage of remifentanil is in order to suppress the hemodynamic response to endotracheal intubation. The methods of administration are a bolus injection, an injection of a loading dose with a continuous infusion, and a continuous infusion. For the induction of anesthesia using propofol and rocuronium, Hall et al. [13] administered a loading dose of remifentanil 0.5 μg/kg and then they continuously infused 0.25 μg/kg/min. Shim et al. [2] reported that continuously infusing remifentanil at 0.2 μg/kg/min effectively suppressed the stimulus-caused increase in blood pressure and heart rate. Their results show that the amount of remifentanil administered until endotracheal intubation was important for inhibiting the hemodynamic response regardless of the method of administration. The optimal dose was normally 1-1.5 μg/kg. This current study followed the methodology of the study by Shim et al. [2] by inducing anesthesia for 6-7 minutes until endotracheal intubation. Thus, we were able to avoid side effects such as muscle rigidity induced by a bolus injection of remifentanil [14,15]. There have been many studies done on the effects of smoking on the cardiovascular system. According to McVeigh et al. [16], the resting heart rate was higher in smokers than in nonsmokers. They also reported that the systolic and diastolic pressures and the MAP were lower in smokers than those in nonsmokers. In a study on only women, Laxton et al. [6] asserted that heart rate of smokers immediately after intubation was significantly greater than that of nonsmokers. Yet Jee and Fig. 2. Changes of the mean arterial pressure (MAP, A) and heart rate (HR, B) in women. The HRs during postintubation period were increased compared with baseline in each group (P < 0.05), but there were no differences between the two groups. Group FS: female smokers, Group FN: female nonsmokers, B: baseline, BO: on unconsciousness, BI: just before intubation, P0: just after intubation, P1, 2, 3: 1, 2, 3 minutes after intubation, respectively. *P < 0.05 compared with baseline. www.ekja.org 511