右旋美托咪定在蛛网膜下隙阻滞和全麻诱导中的镇静效应及对呼吸、循环影响的临床观察
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摘要
第一部分比较右旋美托咪定与咪达唑仑在蛛网膜下隙阻滞下的镇静效应及对呼吸、循环的影响
目的：在蛛网膜下隙阻滞完善镇痛时比较单次负荷剂量1μg·kg-1右美托咪定和临床推荐剂量的咪达唑仑的镇静效应、并以脑电双频指数(BIS)来评估两种药物镇静深度变化,观察两种药物对呼吸、循环的影响。
方法：选择40例ASAⅠ～Ⅱ级,年龄22-60岁,身体质量指数(BMI)19～26kg/m2,拟在蛛网膜下隙阻滞下行下肢手术的择期手术患者。阻滞平面均控制在T10以下,随机分2组,D组(n=20)：右美托咪定1μg·kg-1 10min静脉泵入,M组(n=20)：咪达唑仑50μg·kg-1静脉注射。所有患者均在麻醉前(TO)、脊麻平面固定后(T1)、给药后1 min(T2)、5min(T3)、1 Omin(T4)、20min(T5)、3 Omin(T6)各时间点记录BIS值、警觉/镇静(OAA/S)评分、收缩压(SBP)、舒张压(DBP)、心率(HR)和脉搏血氧饱和度(SPO2)。
结果：D组在T4、T5和T6时间点的BIS值均显著低于M组(77.90±2.90 vs 83.20±3.32,71.30±3.39 vs 82.25±3.64,83.75±2.27 vs 86.70±2.52,p<0.05)；D组在T4、T5和T6时间点的OAA/S评分均明显高于M组(3.05±0.22 vs2.45±0.76,2.70±0.57vs2.60±0.75,3.75±0.55 vs 3.15±0.75,p<0.05)。在T4、T5和T6时间点：D组SBP显著低于M组(105.25±9.34mmHg vs 114.05±10.22mmHg,107.10±8.37mmHg vs 115.85±9.77mmHg,111.65±9.18mmHg vs 118.45±10.12mmHg,p<0.05)；D组DBP显著低于M组(66.10±6.91mmHg vs 74.05±7.92mmHg,68.75±6.81mmHg vs 74.60±6.94mmHg, 71.60±6.86mmHg vs 76.45±6.97mmHg,p<0.05)；D组HR显著低于M组(60.45±2.34次·min-1 vs 71.30±4.78次·min-1,61.40±2.68次·min-1vs72.10±4.49次·min-1,64.35±2.89次·main-1vs74.05±5.09次·min-1,p<0.05)。D组T4、T5和T6时间点的SBP、DBP、HR分别显著低于同组T1时间点(p<0.05)。D组中有4例患者发生SP02<95%,M组中有13例患者发生SP02<95%,呼吸抑制的发生率D组显著低于M组(p<0.05)。
结论：作为蛛网膜下隙阻滞的辅助用药,1μg·kg-1的右美托咪定具有强于临床推荐剂量50μg·kg-1的咪达唑仑的镇静效应,相比于咪达唑仑睡眠中更容易唤醒,且呼吸抑制的发生率低。虽然其血压与心率的下降比较明显,但是仍然在可控范围内。
第二部分右旋美托咪定在全麻诱导和气管插管期的镇静与心血管效应
目的：研究全麻诱导前静脉泵注右美托咪定1μg·kg-1在全麻诱导气管插管期的镇静效应以及对气管插管时血流动力学反应的影响。
方法：选择40例ASAⅠ-Ⅱ级,年龄22-60岁,身体质量指数(BMI)19～26kg/m2,拟在全麻下行腹腔镜手术的择期手术患者随机分2组,每组20例：D组全麻诱导顺序为右美托咪定1μg·kg-1 10min静脉泵入后芬太尼2μg·kg-1静脉注射,F组等量生理盐水(0.9%Nacl)10min静脉泵入后芬太尼4μg·kg-1静脉注射,然后两组患者均使用丙泊酚以血浆药物浓度为靶目标进行靶控输注,靶浓度(Cp)设定为4μg·ml-1,待患者脑电双频指数(BIS)值到达50时注入罗库溴铵0.6mg·kg-1,90s后气管插管,两组患者插管后继续丙泊酚靶控输注观察BIS值的变化。所有患者均在全麻前(T0)、泵入右美托咪定(0.9%Nacl)后5 min(T1)、10 min(T2)、诱导后(T3)、插管即刻(T4)、插管后1min(T5)、插管后3min(T6)、的各时间点记录BIS值、收缩压(SBP)、舒张压(DBP)、心率(HR)以及两组患者BIS值从开始诱导至到达50的时间和BIS达到50时丙泊酚的用量和丙泊酚的效应室浓度(Ce)。
结果：D组在T1、T2、T3、T4、T5和T6各个时间点的BIS值显著低于F组(89.05±5.46 vs 96.15±0.75,79.10±4.73 vs 96.25±0.79,46.00±3.83 vs 51.70±2.36,46.95±4.95 vs52.80±2.57,41.60±5.56 vs 50.95±1.88,38.50±4.65 vs 48.85±2.16,p<0.05)。在T4、T5和T6时间点：D组SBP显著低于F组(116.05±12.57mmHg vs134.05±9.34 mmHg,114.10±9.16 mmHg vs 129.70±12.28mmHg,109.05±8.80mmHg vs 122.70±11.46mmHg,p<0.05)；D组DBP显著低于F组(71.00±9.80mmHg vs 84.55±7.85mmHg,72.05±8.47mmHg vs 82.05±7.57mmHg,68.15±8.50mmHg vs 76.80±6.51mmHg,p<0.05)；D组HR显著低于F组(73.60±16.51次·min-1 vs 93.90±5.10次·min-1,68.95±10.48次·min-1 vs 88.95±5.46次·min-1,66.70±9.10次·min-1 vs 80.00±3.52次·min-1,p<0.05)。两组T4、T5和T6时间点的SBP、DBP、HR均显著高于同组T3时间点(p<0.05)。BIS值降至50时：D组所需的时间明显短于F组(103.55±12.81s vs 145.15±24.93s,p<0.01)；D组丙泊酚的用量明显小于F组(8.05±0.76 ml vs 10.06±1.51ml,p<0.05)；D组丙泊酚的效应室浓度(Ce)显著低于F组(3.04±0.25gg·ml-1 vs 3.32±0.29gg·ml-1,p<0.05)。
结论：全麻诱导前静脉泵注右美托咪定1μg·kg-1,在全麻诱导期有较好的镇静作用,能较好地抑制全麻诱导气管插管期间的心血管反应,血流动力学波动少,全麻诱导的时间短以及全麻诱导期芬太尼、丙泊酚的用量减少等优点,提示右美托咪定与丙泊酚的镇静有协同作用。
Part I Comparison of the sedative effects of dexmedetomidine & midazolam during spinal anesthesia, and their impacts on respiratory & cardiovascular systems
Objective:We studied the sedative effect of a single loading dose (1μg-kg-1) of dexmedetomidine in the procedure of employing subarachnoid block in spinal anesthesia to accomplish analgesia and compared it with that of midazolam in the dosage recommended by clinical trials. We evaluated the sedative effects of these two medications by analyzing the collected BIS data and observed their impacts on respiratory & cardiovascular systems.
Methods:Forty patients in ASA gradeⅠ～Ⅱ, age 20～60 and BMI 19～26 kg/m2, scheduled to undergo lower extremity surgery with subarachnoid block in spinal anesthesia. They were randomly assigned to one of two groups (n=20 each group). Level of anesthesia was controlled beneath Tio. Group D patients received intravenous infusion of 1μg-kg"1 of dexmedetomidine within a 10-minute period. Group M patients were administrated 50μg-kg-1 of midazolam during 10 minutes as well. We collected BIS, OAA/S, SBP, DBP, HR and SPO2 figures of both groups at pre-anesthesia time (TO), when level of anesthesia stabilized (T1),1 minute (T2),5 minutes (T3),10 minutes (T4),20 minutes (T5) and 30 minutes (T6) subsequent to dosing, respectively.
Results:At T4,T5 and T6:BIS of group D patients were significantly lower than those of group M (77.90±2.90 vs 83.20±3.32,71.30±3.39 vs 82.25±3.64,83.75±2.27 vs 86.70±2.52, p<0.05); OAA/S of group D patients were much higher than group M patients (3.05±0.22 vs 2.45±0.76,2.70±0.57 vs 2.60±0.75,3.75±0.55 vs 3.15±0.75, p<0.05). At the corresponding instances (T4, T5 and T6):SBP of group D patients were lower than group M patients (105.25±9.34mmHg vs 114.05±10.22mmHg,107.10±8.37mmHg vs 115.85±9.77mmHg, 11.65±9.18mmHg vs 118.45±10.12mmHg, p<0.05); DBP of group D patients were lower than group M patients were (66.10±6.91mmHg vs 74.05±7.92mmHg,68.75±6.81mmHg vs 74.60±6.94mmHg,71.60±6.86mmHg vs 76.45±6.97mmHg, p<0.05); HR of group D patients were lower than group M patients (60.45±2.34b·min-1 vs 71.30±4.78b-min-1, 61.40±2.68b·min-1 vs 72.10±4.49b·min-1,64.35±2.89b·min-1 vs 74.05±5.09b·min-1, p<0.05). Compared with same group at T1, SBP, DBP, and HR of group D patients went down considerably (p<0.05) at T4, T5 and T6. There were 4 and 13 patients got SPO2<95% in group D and M, respectively. We can see that incidence of minor respiratory depression of group M patients was noticeably higher than that of group D patients (p<0.05).
Conclusions:As an adjuvant medication in the procedure of employing subarachnoid block in spinal anesthesia, the sedative effect of 1μg-kg-1 of dexmedetomidine is stronger than that of 50μg·kg-1 of midazolam,the dosage recommended by clinical trials. Compared with midazolam, patients receiving dexmedetomidine stand a better chance to wake up and have lower incidence of respiratory depression. Although the decreases of blood pressure and heart beat rate are substantial, they are yet in the controllable range.
Part II The sedative effects of dexmedetomidine during general anesthesia induction & tracheal intubation, and its impacts on cardiovascular systems
Objective:Study the sedative effects of dexmedetomidine in the dose of lμg-kg-1 before general anesthesia induction and haemodynamics during tracheal intubation.
Methods:Forty patients in ASA gradeⅠ～Ⅱ, age 20～60, BMI 19～26 kg/m2, scheduled to undergo laparoscopic surgery with general anesthesia. They were randomly assigned to two groups (n=20 each group) as well. Group D patients received intravenous infusion of dexmedetomidine lμg-kg-1 within a period of 10 minutes. Then intravenous infusion of fentanyl 2μg·kg-1. Group F patients, we administrated the same amount of 0.9%Nacl within same time instead of dexmedetomidine before intravenous infusion of fentanyl 4μg·kg-1. Next in two groups we setting plasma concentration as the target and 4μg·ml-1 as the targeting concentration (Cp), we conducted target controlled infusion (TCI) of propofol. We injected 0.6mg·kg-1 of rocuronium when patients'BIS reached 50. In 90 seconds, tracheal intubation was applied. We were monitoring BIS and continued injecting propofol till the targeting plasma concentration was reached. We collected the statistics of BIS, SBP, DBP, HR and at pre-anesthesia time (TO),5 minutes post dosing (T1),10 minutes post dosing (T2), subsequent to induction (T3), at tracheal intubation (T4),1 minute (T5) and 3 minutes (T6) following tracheal intubation, respectively.We logged the time, the amount of propofol required for patients and The propofol effect-site concentration(Ce), when BIS reached 50.
Results:At T1, T2, T3, T4, T5 and T6, BIS of group D were significantly lower than group F patients (89.05±5.46 vs 96.15±0.75,79.10±4.73 vs 96.25±0.79,46.00±3.83 vs 51.70±2.36,6.95±4.95 vs 52.80±2.57,1.60±5.56 vs 50.95±1.88 and 38.50±4.65 vs 48.85±2.16, p<0.05), At the instances of T4, T5 and T6, SBP of group D were noticeably lower than those of group F (116.05±12.57mmHg vs 134.05±9.34mmHg,114.10±9.16mmHg vs 129.70±12.28mmHg,109.05±8.80mmHg vs 122.70±11.46mmHg, p<0.05), respectively; DBP of group D were noticeably lower than group F patients (71.00±9.80mmHg vs 84.55±7.85mmHg, 72.05±8.47mmHg vs 82.05±7.57mmHg,68.15±8.50mmHg vs 76.80±6.51mmHg, p<0.05), HR of group D significantly lower than group F(73.60±16.51b-min-1vs 93.90±5.10b-min-1, 68.95±10.48b-min-1 vs 88.95±5.46b-min-1,66.7±9.10b-min-1 vs 80.00±3.52b-min-1, p<0.05). Comparing with same group at T3, figures were considerably higher at T4,T5 and T6 for both groups of patients (p<0.05). For patients to reach BIS of 50, it took (103.55±12.81s vs 145.15±24.93s, p<0.01) for group D and F, it took (8.05±0.76ml vs 10.06±1.51ml, p<0.05) of propofol for group D and F, The effect-site concentration of propofol (Ce) for group D and F (3.04±0.25μg·ml-1 vs 3.32±0.29μg·ml-1, p<0.05), respectively; group D were significantly lower than group F.
Conclusions:Applied prior to general anesthesia induction, 1μg·kg-1 of dexmedetomidine has enhanced sedative effect during general anesthesia. Dexmedetomidine effectively suppresses adverse cardiovascular reactions and mitigates haemodynamics during tracheal intubation in general anesthesia induction. It also shortens the time to achieve general anesthesia induction, decreases the amount of fentanyl and propofol in general anesthesia, and works with propofol complementarily.
目的：在蛛网膜下隙阻滞完善镇痛时比较单次负荷剂量1μg·kg-1右美托咪定和临床推荐剂量的咪达唑仑的镇静效应、并以脑电双频指数(BIS)来评估两种药物镇静深度变化,观察两种药物对呼吸、循环的影响。
方法：选择40例ASAⅠ～Ⅱ级,年龄22-60岁,身体质量指数(BMI)19～26kg/m2,拟在蛛网膜下隙阻滞下行下肢手术的择期手术患者。阻滞平面均控制在T10以下,随机分2组,D组(n=20)：右美托咪定1μg·kg-1 10min静脉泵入,M组(n=20)：咪达唑仑50μg·kg-1静脉注射。所有患者均在麻醉前(TO)、脊麻平面固定后(T1)、给药后1 min(T2)、5min(T3)、1 Omin(T4)、20min(T5)、3 Omin(T6)各时间点记录BIS值、警觉/镇静(OAA/S)评分、收缩压(SBP)、舒张压(DBP)、心率(HR)和脉搏血氧饱和度(SPO2)。
结果：D组在T4、T5和T6时间点的BIS值均显著低于M组(77.90±2.90 vs 83.20±3.32,71.30±3.39 vs 82.25±3.64,83.75±2.27 vs 86.70±2.52,p<0.05)；D组在T4、T5和T6时间点的OAA/S评分均明显高于M组(3.05±0.22 vs2.45±0.76,2.70±0.57vs2.60±0.75,3.75±0.55 vs 3.15±0.75,p<0.05)。在T4、T5和T6时间点：D组SBP显著低于M组(105.25±9.34mmHg vs 114.05±10.22mmHg,107.10±8.37mmHg vs 115.85±9.77mmHg,111.65±9.18mmHg vs 118.45±10.12mmHg,p<0.05)；D组DBP显著低于M组(66.10±6.91mmHg vs 74.05±7.92mmHg,68.75±6.81mmHg vs 74.60±6.94mmHg, 71.60±6.86mmHg vs 76.45±6.97mmHg,p<0.05)；D组HR显著低于M组(60.45±2.34次·min-1 vs 71.30±4.78次·min-1,61.40±2.68次·min-1vs72.10±4.49次·min-1,64.35±2.89次·main-1vs74.05±5.09次·min-1,p<0.05)。D组T4、T5和T6时间点的SBP、DBP、HR分别显著低于同组T1时间点(p<0.05)。D组中有4例患者发生SP02<95%,M组中有13例患者发生SP02<95%,呼吸抑制的发生率D组显著低于M组(p<0.05)。
结论：作为蛛网膜下隙阻滞的辅助用药,1μg·kg-1的右美托咪定具有强于临床推荐剂量50μg·kg-1的咪达唑仑的镇静效应,相比于咪达唑仑睡眠中更容易唤醒,且呼吸抑制的发生率低。虽然其血压与心率的下降比较明显,但是仍然在可控范围内。
第二部分右旋美托咪定在全麻诱导和气管插管期的镇静与心血管效应
目的：研究全麻诱导前静脉泵注右美托咪定1μg·kg-1在全麻诱导气管插管期的镇静效应以及对气管插管时血流动力学反应的影响。
方法：选择40例ASAⅠ-Ⅱ级,年龄22-60岁,身体质量指数(BMI)19～26kg/m2,拟在全麻下行腹腔镜手术的择期手术患者随机分2组,每组20例：D组全麻诱导顺序为右美托咪定1μg·kg-1 10min静脉泵入后芬太尼2μg·kg-1静脉注射,F组等量生理盐水(0.9%Nacl)10min静脉泵入后芬太尼4μg·kg-1静脉注射,然后两组患者均使用丙泊酚以血浆药物浓度为靶目标进行靶控输注,靶浓度(Cp)设定为4μg·ml-1,待患者脑电双频指数(BIS)值到达50时注入罗库溴铵0.6mg·kg-1,90s后气管插管,两组患者插管后继续丙泊酚靶控输注观察BIS值的变化。所有患者均在全麻前(T0)、泵入右美托咪定(0.9%Nacl)后5 min(T1)、10 min(T2)、诱导后(T3)、插管即刻(T4)、插管后1min(T5)、插管后3min(T6)、的各时间点记录BIS值、收缩压(SBP)、舒张压(DBP)、心率(HR)以及两组患者BIS值从开始诱导至到达50的时间和BIS达到50时丙泊酚的用量和丙泊酚的效应室浓度(Ce)。
结果：D组在T1、T2、T3、T4、T5和T6各个时间点的BIS值显著低于F组(89.05±5.46 vs 96.15±0.75,79.10±4.73 vs 96.25±0.79,46.00±3.83 vs 51.70±2.36,46.95±4.95 vs52.80±2.57,41.60±5.56 vs 50.95±1.88,38.50±4.65 vs 48.85±2.16,p<0.05)。在T4、T5和T6时间点：D组SBP显著低于F组(116.05±12.57mmHg vs134.05±9.34 mmHg,114.10±9.16 mmHg vs 129.70±12.28mmHg,109.05±8.80mmHg vs 122.70±11.46mmHg,p<0.05)；D组DBP显著低于F组(71.00±9.80mmHg vs 84.55±7.85mmHg,72.05±8.47mmHg vs 82.05±7.57mmHg,68.15±8.50mmHg vs 76.80±6.51mmHg,p<0.05)；D组HR显著低于F组(73.60±16.51次·min-1 vs 93.90±5.10次·min-1,68.95±10.48次·min-1 vs 88.95±5.46次·min-1,66.70±9.10次·min-1 vs 80.00±3.52次·min-1,p<0.05)。两组T4、T5和T6时间点的SBP、DBP、HR均显著高于同组T3时间点(p<0.05)。BIS值降至50时：D组所需的时间明显短于F组(103.55±12.81s vs 145.15±24.93s,p<0.01)；D组丙泊酚的用量明显小于F组(8.05±0.76 ml vs 10.06±1.51ml,p<0.05)；D组丙泊酚的效应室浓度(Ce)显著低于F组(3.04±0.25gg·ml-1 vs 3.32±0.29gg·ml-1,p<0.05)。
结论：全麻诱导前静脉泵注右美托咪定1μg·kg-1,在全麻诱导期有较好的镇静作用,能较好地抑制全麻诱导气管插管期间的心血管反应,血流动力学波动少,全麻诱导的时间短以及全麻诱导期芬太尼、丙泊酚的用量减少等优点,提示右美托咪定与丙泊酚的镇静有协同作用。
Part I Comparison of the sedative effects of dexmedetomidine & midazolam during spinal anesthesia, and their impacts on respiratory & cardiovascular systems
Objective:We studied the sedative effect of a single loading dose (1μg-kg-1) of dexmedetomidine in the procedure of employing subarachnoid block in spinal anesthesia to accomplish analgesia and compared it with that of midazolam in the dosage recommended by clinical trials. We evaluated the sedative effects of these two medications by analyzing the collected BIS data and observed their impacts on respiratory & cardiovascular systems.
Methods:Forty patients in ASA gradeⅠ～Ⅱ, age 20～60 and BMI 19～26 kg/m2, scheduled to undergo lower extremity surgery with subarachnoid block in spinal anesthesia. They were randomly assigned to one of two groups (n=20 each group). Level of anesthesia was controlled beneath Tio. Group D patients received intravenous infusion of 1μg-kg"1 of dexmedetomidine within a 10-minute period. Group M patients were administrated 50μg-kg-1 of midazolam during 10 minutes as well. We collected BIS, OAA/S, SBP, DBP, HR and SPO2 figures of both groups at pre-anesthesia time (TO), when level of anesthesia stabilized (T1),1 minute (T2),5 minutes (T3),10 minutes (T4),20 minutes (T5) and 30 minutes (T6) subsequent to dosing, respectively.
Results:At T4,T5 and T6:BIS of group D patients were significantly lower than those of group M (77.90±2.90 vs 83.20±3.32,71.30±3.39 vs 82.25±3.64,83.75±2.27 vs 86.70±2.52, p<0.05); OAA/S of group D patients were much higher than group M patients (3.05±0.22 vs 2.45±0.76,2.70±0.57 vs 2.60±0.75,3.75±0.55 vs 3.15±0.75, p<0.05). At the corresponding instances (T4, T5 and T6):SBP of group D patients were lower than group M patients (105.25±9.34mmHg vs 114.05±10.22mmHg,107.10±8.37mmHg vs 115.85±9.77mmHg, 11.65±9.18mmHg vs 118.45±10.12mmHg, p<0.05); DBP of group D patients were lower than group M patients were (66.10±6.91mmHg vs 74.05±7.92mmHg,68.75±6.81mmHg vs 74.60±6.94mmHg,71.60±6.86mmHg vs 76.45±6.97mmHg, p<0.05); HR of group D patients were lower than group M patients (60.45±2.34b·min-1 vs 71.30±4.78b-min-1, 61.40±2.68b·min-1 vs 72.10±4.49b·min-1,64.35±2.89b·min-1 vs 74.05±5.09b·min-1, p<0.05). Compared with same group at T1, SBP, DBP, and HR of group D patients went down considerably (p<0.05) at T4, T5 and T6. There were 4 and 13 patients got SPO2<95% in group D and M, respectively. We can see that incidence of minor respiratory depression of group M patients was noticeably higher than that of group D patients (p<0.05).
Conclusions:As an adjuvant medication in the procedure of employing subarachnoid block in spinal anesthesia, the sedative effect of 1μg-kg-1 of dexmedetomidine is stronger than that of 50μg·kg-1 of midazolam,the dosage recommended by clinical trials. Compared with midazolam, patients receiving dexmedetomidine stand a better chance to wake up and have lower incidence of respiratory depression. Although the decreases of blood pressure and heart beat rate are substantial, they are yet in the controllable range.
Part II The sedative effects of dexmedetomidine during general anesthesia induction & tracheal intubation, and its impacts on cardiovascular systems
Objective:Study the sedative effects of dexmedetomidine in the dose of lμg-kg-1 before general anesthesia induction and haemodynamics during tracheal intubation.
Methods:Forty patients in ASA gradeⅠ～Ⅱ, age 20～60, BMI 19～26 kg/m2, scheduled to undergo laparoscopic surgery with general anesthesia. They were randomly assigned to two groups (n=20 each group) as well. Group D patients received intravenous infusion of dexmedetomidine lμg-kg-1 within a period of 10 minutes. Then intravenous infusion of fentanyl 2μg·kg-1. Group F patients, we administrated the same amount of 0.9%Nacl within same time instead of dexmedetomidine before intravenous infusion of fentanyl 4μg·kg-1. Next in two groups we setting plasma concentration as the target and 4μg·ml-1 as the targeting concentration (Cp), we conducted target controlled infusion (TCI) of propofol. We injected 0.6mg·kg-1 of rocuronium when patients'BIS reached 50. In 90 seconds, tracheal intubation was applied. We were monitoring BIS and continued injecting propofol till the targeting plasma concentration was reached. We collected the statistics of BIS, SBP, DBP, HR and at pre-anesthesia time (TO),5 minutes post dosing (T1),10 minutes post dosing (T2), subsequent to induction (T3), at tracheal intubation (T4),1 minute (T5) and 3 minutes (T6) following tracheal intubation, respectively.We logged the time, the amount of propofol required for patients and The propofol effect-site concentration(Ce), when BIS reached 50.
Results:At T1, T2, T3, T4, T5 and T6, BIS of group D were significantly lower than group F patients (89.05±5.46 vs 96.15±0.75,79.10±4.73 vs 96.25±0.79,46.00±3.83 vs 51.70±2.36,6.95±4.95 vs 52.80±2.57,1.60±5.56 vs 50.95±1.88 and 38.50±4.65 vs 48.85±2.16, p<0.05), At the instances of T4, T5 and T6, SBP of group D were noticeably lower than those of group F (116.05±12.57mmHg vs 134.05±9.34mmHg,114.10±9.16mmHg vs 129.70±12.28mmHg,109.05±8.80mmHg vs 122.70±11.46mmHg, p<0.05), respectively; DBP of group D were noticeably lower than group F patients (71.00±9.80mmHg vs 84.55±7.85mmHg, 72.05±8.47mmHg vs 82.05±7.57mmHg,68.15±8.50mmHg vs 76.80±6.51mmHg, p<0.05), HR of group D significantly lower than group F(73.60±16.51b-min-1vs 93.90±5.10b-min-1, 68.95±10.48b-min-1 vs 88.95±5.46b-min-1,66.7±9.10b-min-1 vs 80.00±3.52b-min-1, p<0.05). Comparing with same group at T3, figures were considerably higher at T4,T5 and T6 for both groups of patients (p<0.05). For patients to reach BIS of 50, it took (103.55±12.81s vs 145.15±24.93s, p<0.01) for group D and F, it took (8.05±0.76ml vs 10.06±1.51ml, p<0.05) of propofol for group D and F, The effect-site concentration of propofol (Ce) for group D and F (3.04±0.25μg·ml-1 vs 3.32±0.29μg·ml-1, p<0.05), respectively; group D were significantly lower than group F.
Conclusions:Applied prior to general anesthesia induction, 1μg·kg-1 of dexmedetomidine has enhanced sedative effect during general anesthesia. Dexmedetomidine effectively suppresses adverse cardiovascular reactions and mitigates haemodynamics during tracheal intubation in general anesthesia induction. It also shortens the time to achieve general anesthesia induction, decreases the amount of fentanyl and propofol in general anesthesia, and works with propofol complementarily.
引文
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[3]Bhana N, Goa KL, Mcclellan KJ. Dexmedetomidine [J]. Drugs,2000,59(2):263-268.
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