Recently, several studies have shown that the H2-receptor blockers can cause inhibition of cholinesstrase and neuromuscular blockade which suggest involvement of ion-chennel block in relatively large experimental dose. We investigated the effect of three H2-receptor blockers cimetidine, ranitidine, and famotidine on antagonism of vecuronium neuromuscular blockade. Forty ASA class 1 or 2 adult patients were studied. All patients were premedicated with hydroxyzine 1.5mg/kg and glycopyrrolat 0.2mg IM, 1hour before induction. Anesthesia was induced with thiopental sodium 5~6 mg/kg, succinylcholine 1mg/kg and was maintained with 02-N20(50%)-enflurane. Intraoperative muscle relaxation was maintained below 5% of control twitch height on TOF stimulation by combined bolus IV(0.08mg/kg) and contino=uous infusion(0.08mg/kg/hour) of vecuronium. Patients were divided into four groups according to use of H2-receptor blocker just after stop of vecuronium infusion as follows: Control group (n=10): no use of H2-receptor blocker, Cimetidine group (n=10): cimetidine 200mg IV, Rantitidine group (n=10): rantidine 50 mg IV, Famotidine group (n=10): famotidine 50 mg IV. Reversal of neuromuscular blockade with neostigmine(0.04mg/kg) was performed at 10% recovery of first twitch height (T1) in all cases. The recovery of T1 and T4 ratio after reversal was measured at 1min, interval for 20 min. The results were as follows: 1) The recovery of twitch height after administration of neostigmine was prolonged in all three H2-receptor blocker groups as compared to control group, but statistical significance was noted only in Famotidine group (p<0.05). 2) The changes of heart rate and mean arterial pressure after administration of neostigmine were similar in all groups.