蛛网膜下腔与硬膜外腔阻滞对大鼠丙泊酚镇静作用的影响

摘要

目的 观察利多卡因蛛网膜下腔与硬膜外腔阻滞对大鼠丙泊酚镇静作用的影响.方法 40只雄性SD大鼠随机分为四组:蛛网膜下腔利多卡因组(SL组)、蛛网膜下腔生理盐水组(SS组)、硬膜外利多卡因组(EL组)和硬膜外生理盐水组(ES组),每组10只.建立大鼠蛛网膜下腔和硬膜外腔阻滞模型,SL组和SS组分别经蛛网膜下腔注射2%利多卡因201μL和生理盐水201μL;EL组和ES组分别经硬膜外腔注射2%利多卡因70μL和生理盐水70μL;随后经尾静脉泵注丙泊酚,比较四组大鼠眼睑反射消失时丙泊酚的用量.用钳夹法测定并比较蛛网膜下腔与硬膜外腔阻滞平面.结果 40只雄性SD大鼠行蛛网膜下腔和硬膜外腔置管后,8只大鼠因模型失败剔除实验.SL组使大鼠眼睑反射消失的丙泊酚用量(7.61±0.81)mg·kg-1,n=8明显少于SS组(10.13±1.07)mg·kg-1,n=8,P＜0.01;EL组使大鼠眼睑反射消失的丙泊酚用量(7.33±1.01)mg·kg-1,n=8明显少于ES水组(10.40±1.05)mg·kg-1,n=8,P＜0.01;而SL组和EL组及SS组和ES组的丙泊酚用量,差异无统计学意义(P＞0.05).SL组和EL组的阻滞平面分别为剑突下(1.5±0.7)cm和(1.2±0.5)cm,二组间比较差异无统计学意义(P＞0.05).结论 利多卡因蛛网膜下腔和硬膜外腔阻滞均能减少大鼠丙泊酚镇静催眠用量.%Objective To investigate the effects of spinal and epidural lidocaine block on sedation of propofol in rats.Methods 48 Sprague -Dawley (SD) rats were randomly divided into Subarachnoid lidocaine group (SL group), Subarachnoid normal saline group (SS group), Epidural lidocaine group (EL group) and Epidural normal saline group (ES group).The rats respectively received 20μL of 2％ lidocaine, or normal saline; and 70μL of 2％ lidocaine, or normal saline intrathecally in four groups.The dosage of propofol required to ablate the eyelid reflex and compared among four groups.The level of sensory block was assessed with pinch stimulation and compared the level between SL group and EL group.Results There were 32 rats included in this study after intrathecal catheter placement.The dosage of propofol required to ablate the eyelid reflex in SL group (7.61 ± 0.81 )mg · kg-1, n = 8, EL group (7.33 ± 1.O1 ) mg · kg-1, n = 8, were significantly decreased comparing with intrathecally administered normal saline group ( 10.13 + 1.07 ) mg · kg-1, n = 8,(10.40 ± 1.05 ) mg · kg-1, n = 8 (P ＜ O.0001 ).Spinal anesthesia level of rats in SL group and EL group were respectively ( 1.5 ± 0.7) cm and ( 1.2 ± O.5 ) cm below xiphoid process ( P ＞ 0.05 ).Conclusion Spinal and epidural block can reduce propofol requirement to ablate the eyelid reflex in rats.Most speculated mechanism for sedation during subarachnoid block is the indirect central effect of spinal deafferentation.