Nimodipine, a calcium channel blocking drug, is used in the treatment of cerebral arterial spasm after subarachnoid haemorrhage due to bleeding from an intracranial aneurysm. The purpose of this study was to evaluate the effects of nimodipine on neuromuscular blockade after vecuronium had been given to facilitate tracheal intubation and maintenance of muscle paralysis in patients undergoing clipping of intracranial aneurysm. Twenty patients were divided into two groups: a control group (n = 10) who received no calcium channel blocking drug, and a nimodipine group (n = 10) consisting of patients treated with nimodipine at clinically used doses of 0.03 mg kg(-1) h(-1) pre- and perioperatively. Anaesthesia was induced with atropine 10 microg kg(-1), dehydrobenzperidol 5 mg, fentanyl 5 microg kg(-1), thiopental 5 mg kg(-1) and maintained with a mixture of N2O and isoflurane (0.5-1% inspired concentration) in O2, and additional doses of fentanyl 2.5 microg kg(-1). Neuromuscular responses were monitored by acceleromyograpy. The first twitch of the train-of-four response (T1) was considered as twitch height. After a stabilization period, an intubating dose of vecuronium 0.1 mg kg(-1) was administered. The onset of action, the time of first appearance of T1 and clinical duration of action were recorded. Then, maintenance doses of vecuronium 0.03 mg kg(-1) were administered twice more when T1 had recovered to 25% of control twitch height. The study ended when the recordings of the 3rd 25% T1 recovery had been obtained. There were no statistical differences in the onset time (120+/-44 s in the control group, 141+/-33 s in the nimodipine group), in the first appearance time of T1 (28+/-6 min in the control group, 30+/-8 min in the nimodipine group), and in the times for 25% recovery in T1 (41+/-11, 32+/-2, 40+/-13 min in the control group, respectively, and 44+/-16, 36+/-15, 38+/-15 min in nimodipine group, respectively) between the groups studied. The time between the injection of the intubating dose of vecuronium and the third recovery of T1-25% of control was not significantly different between the control group (113+/-34 min) and the nimodipine group (117+/-42 min). This study indicates that nimodipine does not have any significant effect on the time course of action of vecuronium including the onset time and its clinical duration of action after the initial and the two maintenance doses in these patients.

Nimodipine, a calcium channel blocking drug, is used in the treatment of cerebral arterial spasm after subarachnoid haemorrhage due to bleeding from an intracranial aneurysm. The purpose of this study was to evaluate the effects of nimodipine on neuromuscular blockade after vecuronium had been given to facilitate tracheal intubation and maintenance of muscle paralysis in patients undergoing clipping of intracranial aneurysm. Twenty patients were divided into two groups: a control group (n 10) who received no calcium channel blocking drug, and a nimodipine group (n 10) consisting of patients treated with nimodipine at clinically used doses of 0.03 mg kg À1 h À1 pre-and perioperatively. Anaesthesia was induced with atropine 10 mg kg À1 , dehydrobenzperidol 5 mg, fentanyl 5 mg kg À1 , thiopental 5 mg kg À1 and maintained with a mixture of N 2 O and iso¯urane (0.5±1% inspired concentration) in O 2 , and additional doses of fentanyl 2.5 mg kg À1 . Neuromuscular responses were monitored by acceleromyograpy. The ®rst twitch of the train-offour response (T 1 ) was considered as twitch height. After a stabilization period, an intubating dose of vecuronium 0.1 mg kg À1 was administered. The onset of action, the time of ®rst appearance of T 1 and clini-cal duration of action were recorded. Then, maintenance doses of vecuronium 0.03 mg kg À1 were administered twice more when T 1 had recovered to 25% of control twitch height. The study ended when the recordings of the 3rd 25% T 1 recovery had been obtained. There were no statistical differences in the onset time (120 44 s in the control group, 141 33 s in the nimodipine group), in the ®rst appearance time of T 1 (28 6 min in the control group, 30 8 min in the nimodipine group), and in the times for 25% recovery in T 1 (41 11, 32 2, 40 13 min in the control group, respectively, and 44 16, 36 15, 38 15 min in nimodipine group, respectively) between the groups studied. The time between the injection of the intubating dose of vecuronium and the third recovery of T 1 À25% of control was not signi®cantly different between the control group (113 34 min) and the nimodipine group (117 42 min). This study indicates that nimodipine does not have any signi®cant effect on the time course of action of vecuronium including the onset time and its clinical duration of action after the initial and the two maintenance doses in these patients.