Objective To investigate the effect of diabetes mellitus on neuromuscular blocking effect of cisatracurium in patients. Methods Forty ASA Ⅱ patients, aged 30-64 yr, weighing 44-90 kg, scheduled for neurosurgical operation under general anesthesia, were assigned into 2 groups (n = 20 each): type 2 diabetes mellitus group (group D) and non-diabetes mellitus group (group ND). General anesthesia was induced with midazolam,fentanyl and etomidate. Neuromuscular block was assessed with Epoch XP nerve electrophysiology monitor. A train-of-four stimulation of ulnar nerve was used. Cisatracurium 0.15 mg/kg was injected intravenously over 5 s after T1 was maintained at 100%. Tracheal intubation was performed after the onset of the muscle relaxant. Anesthesia was maintained with iv infusion of propofol 4-8 mg· kg - 1 · h - 1 and remifentanil 0.1-0.3μg· kg - 1 · min - 1. The effect of inmbation was evaluated and graded. The onset time, clinical duration, recovery time and recovery index were recorded. Results The onset time was significantly longer in group D than in group ND ( P ＜ 0.05). There was no significant difference in the clinical duration, recovery time and recovery index and intubation effect grade between the two groups ( P ＞ 0.05). Conclusion Diabetes can prolong the onset time of cisatracurium, but has no effect on the clinical duration and recovery time.

Objective To evaluate the effect of hypothermia on somatosensory evoked potentials (SSEPs). Methods Thirteen ASA Ⅱ or Ⅲ patients aged 23-51 yr weighing 45-82 kg scheduled for cardiac surgery were enrolled in this study. Bilateral median nerve SSEPs (N9, N13, N20) were recorded after induction.The MAP, peak latency and amplitude of N9, N13 and N20 were recorded when the target temperature (36, 35,34, 33 ℃ ) was reached during the cooling and rewarming periods. The neurological dysfunction was recorded after operation. Results The peak latency was prolonged and MAP was decreased with the decrease in the body temperature during the cooling period, the peak latency was shortened with the increase in the body temperature during the rewarming period ( P ＜ 0.05), but no significant change in the amplitudes was found ( P ＞ 0.05). The regression equation of the interaction between the peak latency and body temperature was YN9= -0.558X + 28.994(r=-0.673), YN13 =-1.121X+53.242 (r= -0.702) , YN20 = -1.458X+72.036(r= -0.702) during the cooling period (P ＜ 0.05), and YN9 = - 0.505X + 27.313 ( r = - 0.634), YN13 = - 0.905X + 46.249(r= -0.619), YN20 = - 1.142X + 61.668 (r= -0.600) during the rewarming period (P ＜0.05). No neurological dysfunction was found in all the patients. Conclusion Hypothermia can prolong the peak latency of SSEP and does not alter the SSEP amplitude.