乙咪酯全身及鞘内用药对蜜蜂毒诱致大鼠热和机械性痛敏的抑制作用

Effects of intravenous and/or intrathecal etomidate on thermal and mechanical hyperalgesia induced by intraplantar injection of bee venum in rats

目的 研究乙咪酯是否对热和机械性痛敏具有抑制作用。方法 静脉、鞘内或联合用药 ,观察乙咪酯对蜜蜂毒所致热和机械性痛敏的影响。结果 (大鼠一侧足底注入蜜蜂毒 3h后注射部位机械刺激反应阈值降低了 89% ,热刺激反应潜伏期缩短了 86 % ;对侧热刺激反应潜伏期缩短了34%。 (与致敏组比较 ,乙咪酯静脉 (1 2 84mg/kg)或鞘内 (2 0 μg/10 μl)预处理使蜜蜂毒注射后 3h两侧足底热刺激反应潜伏期延长 (P <0 0 5 ) ;鞘内预处理联合 4h后相同剂量静脉或鞘内再处理进一步延长 ;仅鞘内预处理联合 4h后静脉再处理组机械刺激反应阈值显著提高 (P <0 0 5 )。结论 乙咪酯对蜜蜂毒诱致的原发和继发性热痛敏有剂量累积性抑制 ;

Objective To investigate whether etomidate (E) has any suppressive effects on hyperalgesia induced by intraplantar subcutaneous injection of bee venum (BV) Methods BV was injected into the plantar surface of one hind paw to produce hyperalgesia Pain was estimated by measuring withdrawal response latency of the hindpaw to radiant heat and withdrawal threshold to von Frey filament of different stimulation intensity (40 580mN) Both injected and contralateral hind paw were tested 36 adult male and female SD rats weighing 180 250g were randomly divided into 6 groups of 6 rats each: group C 1:normal control; group C 2: hyperalgesia induced by BV; group V: intravenous E 1 28mg/kg before BV induced hyperalgesia; group T: intrathecal E 20μg/10μl before BV induced hyperalgesia; group TT: intrathecal E 20μg/10μl before induced hyperalgesia + intrathecal E 20μg/10μl 4h after induced hyperalgesia; group TV: intrathecal E 20μg/10μl before induced hyperalgesia + intravenous E 1 28mg/kg 4h after induced hyperalgesia Intrathecal E was given through an implanted spinal cannulae Pain response was measured 2 h after BV induced hyperalgesia in group C 2, V and T and 4 h after BV induced hyperalgesia in group TT and TV Results ① Intraplantar injection of BV not only made the withdrawal latency of the injected hindpaw to heat stimulation drop by 86% and withdrawal threshold to mechanical stimulation drop by 89% but also reduced the withdrawal latency of the contralateral hindpaw to heat stimulation by 34% ② Either intravenous or intrathecal pretreatment with etomidate significantly prolonged the withdrawal latency to heat stimulation after intraplantar BV injection Withdrawal latency to heat stimulation was further prolonged by intravenous or intrathecal etomidate given after BV induced hyperalgesia Withdrawal threshold to mechanical von Frey filament stimulation was increased significantly only by intrathecal etomidate pretreatment combined with intravenous etomidate given after BV induced hyperalgesia Conclusions Etomidate has suppressive effects on the primary and secondary BV induced thermal hyperalgesia in a dose accumulative manner The mechanism of suppressive effect of etomidate on BV induced mechanical hyperalgesia is not confined to spinal cord