Huntoon M, Eisenach J C, Boese P
Department of Anesthesiology, Portsmouth Naval Medical Center, Virginia.
Anesthesiology. 1992 Feb;76(2):187-93. doi: 10.1097/00000542-199202000-00005.
Epidurally administered clonidine represents a new approach to postcesarean section pain therapy, yet the appropriate bolus dose and infusion to provide effective pain relief have not been defined. In addition, whether 2-chloroprocaine, a commonly used local anesthetic for intraoperative anesthesia, interferes with clonidine's analgesia, as it does with that of opioids, has not been examined. In this study, using a randomized, blinded design, 63 women received either bupivacaine or 2-chloroprocaine for epidural anesthesia for cesarean section and then received, upon request for analgesia in the recovery room, epidural clonidine 400 micrograms or 800 micrograms bolus, each followed by a 24-h infusion of 40 micrograms/h, or an equivalent volume bolus and infusion of saline. In the bupivacaine group, both clonidine doses produced equivalent analgesia, as determined by pain scores and time to first supplemental intravenous morphine request, and sustained analgesia was produced by clonidine infusion, as measured by need for supplemental morphine. In contrast, 2-chloroprocaine diminished analgesia from 800 micrograms by 21% and abolished analgesia from 400 micrograms clonidine. After 2-chloroprocaine, sustained analgesia from continuous clonidine infusion was present only in the group who had received 800 micrograms clonidine. Clonidine did not alter resolution of residual local anesthetic sensory blockade, as measured by 2- or 4-segment regression following either local anesthetic, but did prolong duration of motor blockade in women receiving bupivacaine. Clonidine produced small decreases in heart rate and blood pressure. One patient received iv fluids for hypotension; one had asymptomatic bradycardia resolving without therapy; and one had mild hypoxemia with snoring during clonidine-induced sedation, responding to supplemental oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)
硬膜外给予可乐定是剖宫产术后疼痛治疗的一种新方法,但尚未确定能提供有效疼痛缓解的合适推注剂量和输注方案。此外,常用的术中麻醉局部麻醉药2-氯普鲁卡因是否会像干扰阿片类药物的镇痛作用那样干扰可乐定的镇痛作用,尚未得到研究。在本研究中,采用随机、双盲设计,63名妇女在剖宫产硬膜外麻醉时接受布比卡因或2-氯普鲁卡因,然后在恢复室要求镇痛时,接受硬膜外注射400微克或800微克可乐定,随后以40微克/小时的速度进行24小时输注,或给予等量推注和输注生理盐水。在布比卡因组中,根据疼痛评分和首次要求补充静脉注射吗啡的时间判断,两种可乐定剂量产生的镇痛效果相当,通过补充吗啡的需求来衡量,可乐定输注产生了持续的镇痛作用。相比之下,2-氯普鲁卡因使800微克可乐定的镇痛效果降低了21%,并消除了400微克可乐定的镇痛作用。在使用2-氯普鲁卡因后,仅在接受800微克可乐定的组中存在可乐定持续输注产生的持续镇痛作用。可乐定并未改变残留局部麻醉药感觉阻滞的消退情况,这通过两种局部麻醉药后的2或4节段回归来衡量,但确实延长了接受布比卡因的妇女的运动阻滞持续时间。可乐定使心率和血压略有下降。一名患者因低血压接受静脉输液;一名患者有无症状心动过缓,未经治疗自行缓解;一名患者在可乐定诱导的镇静期间出现轻度低氧血症伴打鼾,经补充氧气后缓解。(摘要截断于250字)