Rosenberg P H, Zou J, Heavner J E
Department of Anaesthesiology, Helsinki University Central Hospital, Finland.
Acta Anaesthesiol Scand. 1993 Nov;37(8):751-5. doi: 10.1111/j.1399-6576.1993.tb03803.x.
In this study, we compared the central nervous system and cardiovascular system toxicity of i.v. administered 0.5% 2-chloroprocaine (N = 10) and 0.5% prilocaine (N = 10) in lightly anaesthetised rats. Arterial blood pressure, ECG and EEG were continuously recorded. Prilocaine produced the predetermined toxic end-points (i.e. seizure activity on EEG, isoelectric EEG, cardiac arrhythmia on ECG, asystole on ECG) at significantly lower doses than 2-chloroprocaine (P < 0.05). The mean dose of prilocaine producing asystole was 166 mg.kg-1 (+/- 45 mg.kg-1, s.d.) vs. 255 mg.kg-1 (+/- 42 mg.kg-1) for 2-chloroprocaine (P < 0.01). The rate of decrease of mean arterial blood pressure during the infusion was significantly faster with prilocaine (P < 0.01). Typically, arrhythmias did not appear until just before asystole, suggesting that neither of the local anaesthetics possessed marker arrhythmogenic properties. It is concluded that prilocaine is slightly more toxic than 2-chloroprocaine in the rat, but that both local anaesthetics have a wide margin of safety. Doses producing seizure activity on the EEG (prilocaine 53 mg.kg-1 and 2-chloroprocaine 70 mg.kg-1, on average) are much higher than those used in clinical practice (usually < 10 mg.kg-1).
在本研究中,我们比较了静脉注射0.5%氯普鲁卡因(N = 10)和0.5%丙胺卡因(N = 10)对轻度麻醉大鼠中枢神经系统和心血管系统的毒性。持续记录动脉血压、心电图和脑电图。丙胺卡因产生预定毒性终点(即脑电图上的癫痫活动、脑电图等电位、心电图上的心律失常、心电图上的心脏停搏)的剂量显著低于氯普鲁卡因(P < 0.05)。导致心脏停搏的丙胺卡因平均剂量为166 mg·kg-1(±45 mg·kg-1,标准差),而氯普鲁卡因的平均剂量为255 mg·kg-1(±42 mg·kg-1)(P < 0.01)。输注期间平均动脉血压的下降速率丙胺卡因显著更快(P < 0.01)。通常,心律失常直到心脏停搏前才出现,这表明两种局部麻醉药均不具有标志性致心律失常特性。结论是,在大鼠中丙胺卡因的毒性略高于氯普鲁卡因,但两种局部麻醉药都有较宽的安全范围。脑电图上产生癫痫活动的剂量(丙胺卡因平均为53 mg·kg-1,氯普鲁卡因平均为70 mg·kg-1)远高于临床实践中使用的剂量(通常<10 mg·kg-1)。