Ｏｂｊｅｃｔｉｖｅ　To determine whether smoking affects minimum alveolar concentrations of sevoflurane that block adrenergic responses(MACBAR) in patients receiving laparoscopic cholecystectomy.　Methods　A total of 90 ASA grade Ⅰ or Ⅱ patients(30-50 years old) receiving laparoscopic cholecystectomy were enrolled in this study, and the patients had 49 smokers and 41 non-smokers. The levels of cytochrome P450 family 2 subfamily E member 1(CYP2E1, a principal enzyme metabolizes sevoflurane) and cotinine (a metabolite of nicotine, a bioactive component in cigarettes) in serum were measured one day before the operation. The patients received similar procedures for the induction of general anesthesia, thereafter, the anesthesia was maintained with sevoflurane. Pneumoperitoneum stimulation was applied to trigger adrenergic responses that were assessed by changes in MAP and HR. Meanwhile, MACBAR was recorded.　Results　HR and MAP were at the same levels between smokers and non-smokers(P＞0.05). As expected, the levels of CYP2E1 and cotinine in serum were significantly higher in smokers than non-smokers(P＜0.05). After general anesthesia was induced, HR and MAP were significantly decreased in both smokers and non-smokers(P＜0.05). Pneumoperitoneum stimulation elevated these parameters more robustly in smokers than non-smokers(P＜0.05). Moreover, MACBAR of sevoflurane and levels of CYP2E1 showed a significant correlation（r=0.51，P<0.05）, and both were higher in smokers than non-smokers(P＜0.05).　Conclusions　Smoking patients had higher levels of CYP2E1, which may accelerate the metabolism of sevoflurance and increase MACBAR.