Nitrous oxide is the least potent and soluble inhalation anesthetics in current u. After 1 minute of administration of nitrous oxide, the alveolar coneentration reaches 60-80% of the inspired concentration and 90-100% within 10-15 minutes. Concentration effect and low solubility of N2O causes rapid increase in the concentration of N in rebreathing (circle-absorber) system. High inflow rate (5-10 L/min) results in a rapid rise in inspired concentration. The purpose of this study is to evaluate the effect of different oxygen inflow rates on excretion of N2O by observing the end-tidal N2O concentration using Capnomac II. ASA class 1 and 2 patients (n=21) undergoing general anesthesia were selected and induced with thiopental sodium 4 mg/Kg and succinylcholine 2 mg/Kg followed by administering N2O and O2 each with 2 L/min with fentanyl, midazolam and pancuronium. Administration of N2O was stopped after about 45 minutes when vital signs and ETCO2 concentration were stable with tidal volume 10 ml/Kg at ventilatory rate of 12/min. Oxygen was given at 4 L/min (group I) and 8 L/min (group II). End-tidal N2O concentration was measured every 15 seconds until 3 mins and every 1 minute thereafter. Pharmacokinetic parameters were obtained for each patient. During recovery, end-tidal N2O concentration decreased exponentially in both groups. The time from the end of N administration of until the moment end-tidal N2O concentration reaches 3% is 16.8 minutes with group A and 8 minutes with group B. Area under curve (AUC) and clearance (CL) were not significantly different between both groups but, volume of distribution at steady states and mean residence time decreased significantly in group II compared to group I. Recovery of N2O is affected by the oxygen inflow rate. Therfore high oxygen inflow rate which accellerates excretion of this poorly soluble anesthetics will hasten patient's recovery.