Crawford Jennifer M, Loadsman John A, Yang Kenny Xf, Kam Peter Ca
1 Department of Anaesthetics, Royal Prince Alfred Hospital, Sydney, NSW, Australia.
2 Sydney Medical School, University of Sydney, Sydney, NSW, Australia.
Anaesth Intensive Care. 2019 Mar;47(2):134-140. doi: 10.1177/0310057X19838731. Epub 2019 May 9.
Clonidine has been used successfully to prolong the duration of action of local anaesthetics in peripheral nerve blocks, but its mechanism of action in this setting remains unclear. Some studies suggest that clonidine exerts a vasoconstrictor effect, limiting the washout of local anaesthetic from its site of deposition. We investigated this potential vasoconstrictor effect, using plasma ropivacaine concentrations as a surrogate measure of vasoconstriction, in patients who received transversus abdominis plane (TAP) blocks with and without clonidine. Eighty women undergoing laparoscopic gynaecological surgery were randomly assigned to receive one of four TAP block solutions: 0.2% ropivacaine (control), ropivacaine with clonidine 2 μg/kg (clonidine), ropivacaine with 1:400,000 adrenaline (adrenaline) or ropivacaine and a subcutaneous injection of clonidine 2 μg/kg (SC clonidine). The primary outcome was total venous plasma ropivacaine concentrations up to 6 h after the block. There were no significant differences in plasma ropivacaine concentrations between the control group and the clonidine group at any timepoint in the study, nor were there differences in either the mean maximum ropivacaine concentration ( C) (1.99 μg/mL versus 2.05 μg/mL, P = 0.712) or the time to maximum concentration ( T) (51.0 min versus 56.0 min, P = 0.537). The SC clonidine group also did not differ significantly from the controls ( C 2.13 μg/mL versus 1.99 μg/mL, P = 0.424; T 43.5 min versus 51.0 min, P = 0.201). Plasma ropivacaine concentrations in the adrenaline group were significantly lower than the controls from 10 to 90 min ( P < 0.003 for each comparison), and the C was less than that of the control group (1.36 μg/mL versus 1.99 μg/mL, P < 0.001) with a longer T (103.5 min versus 51.0 min, P = 0.001). These findings indicate that clonidine at a concentration of 1.35 μg/mL added to ropivacaine for TAP blocks did not produce a reduction in plasma ropivacaine concentrations. This suggests a lack of vasoconstrictor effect during TAP blocks. Further studies should evaluate whether vasoconstriction occurs when clonidine is used at higher concentrations or for other blocks.
可乐定已成功用于延长外周神经阻滞中局部麻醉药的作用时间，但其在此情况下的作用机制仍不清楚。一些研究表明，可乐定具有血管收缩作用，可限制局部麻醉药从其注射部位的清除。我们以血浆罗哌卡因浓度作为血管收缩的替代指标，研究了在接受或未接受可乐定的腹横肌平面（TAP）阻滞患者中这种潜在的血管收缩作用。80例接受腹腔镜妇科手术的女性被随机分配接受四种TAP阻滞溶液之一：0.2%罗哌卡因（对照组）、含2μg/kg可乐定的罗哌卡因（可乐定组）、含1:400,000肾上腺素的罗哌卡因（肾上腺素组）或罗哌卡因加皮下注射2μg/kg可乐定（皮下可乐定组）。主要结局是阻滞后6小时内的总静脉血浆罗哌卡因浓度。在研究的任何时间点，对照组和可乐定组之间的血浆罗哌卡因浓度均无显著差异，平均最大罗哌卡因浓度（C）（1.99μg/mL对2.05μg/mL，P = 0.712）或达到最大浓度的时间（T）（51.0分钟对56.0分钟，P = 0.537）也无差异。皮下可乐定组与对照组之间也无显著差异（C 2.13μg/mL对1.99μg/mL，P = 0.424；T 43.5分钟对51.0分钟，P = 0.201）。肾上腺素组的血浆罗哌卡因浓度在10至90分钟时显著低于对照组（每次比较P < 0.003），且C低于对照组（1.36μg/mL对1.99μg/mL，P < 0.001），T更长（103.5分钟对51.0分钟，P = 0.001）。这些发现表明，在TAP阻滞中，添加到罗哌卡因中的1.35μg/mL可乐定并未使血浆罗哌卡因浓度降低。这表明TAP阻滞期间缺乏血管收缩作用。进一步的研究应评估当使用更高浓度的可乐定或用于其他阻滞时是否会发生血管收缩。
