机构地区:[1]广东省广州市第一人民医院麻醉科,510180 [2]广州中医药大学附属骨伤科医院麻醉科,广州510240
出 处:《广东医学》2012年第16期2479-2483,共5页Guangdong Medical Journal
基 金:广东省医学科研基金资助项目(编号:A2011477);广州市医药卫生科研基金资助项目(编号:201102A213071)
摘 要:目的观察氯胺酮对右美托咪定(Dex)靶控输注患者镇静意识消失时浓度效应关系的影响。方法择期行椎管内麻醉下腹部或下肢手术者共60例(ASAⅠ~Ⅱ级),随机分为D组和KD组,每组30例,每组按Dex靶控浓度的不同随机分为5个亚组(n=6),D组(D1~D5)浓度分别为0.54、0.64、0.76、0.90和1.07 ng/mL;KD组(KD1~KD5)浓度分别是0.30、0.37、0.46、0.57和0.70 ng/mL。监测脑电双频谱指数(BIS)、心率(HR)、平均动脉压(MAP)和脉搏氧饱和度(SpO2)、警觉/镇静(OAA/S)评分和睫毛反射;以呼之不应(OAA/S评分≤2)和睫毛反射消失作为意识消失指标,观察和记录30 min内每组及其亚组患者意识消失的例数及其对应靶浓度,采用概率单位法(Probit)回归分析计算两组的浓度-效应曲线方程及其意识消失的半数有效浓度(EC50)和95%有效浓度(EC95)。结果 D组和KD组中各亚组间随着时间推移和亚组间随着靶浓度增加,意识消失率逐渐上升,BIS值逐渐下降(P<0.05);KD组EC50(0.445 ng/mL)和EC95(0.603 ng/mL)显著低于D组EC50(0.738 ng/mL)和EC95(0.990 ng/mL),KD组量效曲线相对D组平行且左移;与基础值比较,两组第3、4、5亚组15 min后MAP逐渐下降(P<0.05),D组第3、4、5亚组5 min后HR逐渐下降,第1、2亚组10 min后HR下降(P<0.05),KD组第3、4、5亚组于20~30 min HR下降明显(P<0.05)。SpO2不同时间SpO2≥95%,差异无统计学意义(P>0.05)。结论随着Dex靶控输注血浆浓度增加,镇静深度增加,小剂量氯胺酮能够降低Dex意识消失所需的靶浓度,增强其镇静效果。Objective To investigate the effects of ketamine on concentration - response of dexmedetomidine with respect to the loss of consciousness via target - controlled infusion (TCI). Methods Sixty patients ( ASA I - II ) un- dergoing lower abdominal or extremity operations under combined spinal - epidural anesthesia were randomly divided into 2 groups (n = 30 ) : Group D (dexmedetomidine alone) and Group KD (dexmedetomidine and ketamine). Patients in Group D were further randomized to 5 subgroups (n = 6 in each), in which the subjects received dexmedetomidine via TCI at the respective target plasma concentrations of 0. 54, 0. 64, 0. 76, 0. 90 and 1.07 ng/mL. Meanwhile, patients in Group KD were randomized 5 subgroups (n --6 in each), in which the subjects with pretreatment of ketamine 0. 4 mg/kg and sus- tained by 5 izg/kg/min intravenously, received dexmedetomidine via TCI at the respective target plasma concentrations of 0. 30, 0. 37, 0.46, 0. 57 and 0. 70 ng/mL. The loss of response to verbal command ( OAA/S scores ≤ 2) and eyelash stimulation was used as the standard of definite unconsciousness. The number of unconscious patients in each group was recorded during the first 30 mins. Bispectral index ( BIS), heart rate ( HR), blood pressure ( BP), SpO2, OAA/S scores and eyelash stimulation were monitored during the study. A quantal response model ( probit analysis) was used to calculate the concentration - effect curve and predict plasma EC50 and EC95 of dexmedetomidine. Results Dexmedetomidine in- duced significant increase of unconsciousness ratio and reduction of BIS values in concentration - dependent manners ( P 〈 0. 05 ). The EC50 and EC95 of loss of consciousness of dexmedetomidine were 0. 445 ng/mL and 0. 603 ng/mL in GroupKD, which were significantly lower than those (0. 738 ng/mL and 0. 990 ng/mL, respectively) in Group D (P 〈0. 05). A paralleled but left - shift concentration - effect curve was observed in Group KD when compared to that i
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