丙泊酚和普鲁卡因在静脉复合全麻中的比较

目的比较丙泊酚与普鲁卡因静脉复合全麻对血流动力学、术中意识及苏醒过程的影响。方法选择30例择期全麻非颅脑手术病人随机均分为两组：Ⅰ组诱导插管用丙泊酚2mg／kg、维库溴铵0．15mg／kg静注,全麻维持用0．2％丙泊酚静滴;Ⅱ组诱导插管用咪唑安定0．15mg／kg、维库溴铵0．15mg／kg静注,全麻维持用1％普鲁卡因静滴。测量诱导前、诱导后、插管时、术中及拔管前的HR、MAP;记录停药至睁眼及拔管的时间;观察术后恶心发生率,询问术中有无意识存在。结果气管插管时、术中及拔管前Ⅰ组HR、MAP较Ⅱ组稳定,Ⅱ组HR、MAP明显高于术前水平（P〈0．01）;Ⅰ组睁眼及拔管时间均明显短于Ⅱ组（P〈0．01）,且术后恶心率及术中意识发生率Ⅱ组高于Ⅰ组（P〈0．01）。结论丙泊酚静脉全麻比较普鲁卡因,具有诱导快、术中循环动力学稳定、苏醒迅速完全且无术中知晓、术后并发症少等优点。     

倍他洛克用于气管插管期对BIS，ICP和血流动力学的影响

目的：观察长效选择性β受体阻滞剂—倍他洛克（metoprolol．美托洛尔）对丙泊酚麻醉诱导气管内插管期的BIS、ICP和血流动力学影响。方法：随机选择鼻蝶入路垂体瘤切除术病人100例，ASAⅠ-Ⅱ级，分为倍他洛克组（工组）和对照组（Ⅱ组），每组50例。工组於麻醉诱导期静脉注射倍他洛克60μg／kg；Ⅱ组静脉注射等容量生理盐水。麻醉诱导采用丙泊酚2mg/kg、芬太尼3μg／kg、罗库溴铵1mg／kg，OSS／A评分0级施行气管内插管．术中持续监测平均动脉压（MAP），心率（HR），颅内压（ICP）和脑电双频谱指数（BIS）。结果：倍他洛克组与对照组在气管插管后1min时的BIS分别为39±11和58±8，前者与插管前相比无显着性改变，而后者则较插管前有明显增高并延续至插管后5min（P〈0.05，P〈0.01），且其组间的显着性差异延续至插管后15min（P〈0.01）．倍他洛克组与对照组的MAP和HR在插管后3min和5min，均较插管前明显上升，对照组HR分别为89±11bpm和76±12bpm，MAP分别为122±16mmHg和106±18mmhg，倍他洛克组HR分别为81±12bpm和74±8bpm，MAP分别为111±18mmHg和97±17mmHg。两组相比，对照组的血流动力学显着性上升（P〈0.01），且其组间的显着性差异延续至插管后30min（P〈0.05，P〈0，01）。对照组的ICP於插管后3min上升为14．0±2.3mmHg，舆插管前相比有显着性差异（P〈0．05）；插管后5min，15min和30min的ICP分别为14.9±．0mmHg，15．5±2．6mmHg和14.4±2.7mmHg，显着性高於倍他洛克组（P〈0．05，P〈0．01）．两组插管后的ICP舆麻醉前比较均有显着性升高（P〈0。01）。结论：倍他洛克能减低麻醉诱导气管插管期的血流动力学波动和ICP升高，并抑制DIS反跳．     

咪唑安定与丙泊酚对脑电双频指数的影响

目的测定和比较咪唑安定与丙泊酚诱导时半数病人入睡时的脑电双频指数（BIS50）和半数有效量（ED50）。方法选择60例无服用精神药物和镇静催眠药物史、无术前用药的门诊手术病人（ASAⅠ～Ⅱ级），随机均分为咪唑安定组（M组）和丙泊酚组（P组），以半数效量序贯法分别进行咪唑安定与丙泊酚诱导的睡眠观察，以对语言指令和睫毛反射消失为入睡指标，同时记录BIS的变化。对取得的数据以直线回归的方法和加权均数法分别求得咪唑安定、丙泊酚的BIS50和ED50。结果咪唑安定诱导后，术峤病人与入睡病人的BIS值均较用药前的基础值明显下降，但下降幅度在两类病人之间差异无统计学意义，BISso和EDso分别为：77．02（95％可信区间为：71．08～85．86）和0．1237mg／kg（95％可信区间为：0．0990-0．1540mg／kg）。丙泊酚诱导时未睡病人的BIS值下降不明显，而入睡病人的BIS值显著下降，两者之间差异有统计学意义（P〈0．05）。丙泊酚的BIS50和ED50分别是79．17（95％可信区间为：72．08～88．55）和1．0192mg／kg（95％可信区间为：0．9400～1．1480mg／kg）。结论咪唑安定和丙泊酚对BIS的影响有较大的差异。与丙泊酚比较，BIS值与咪唑安定催眠效果的相关性小于丙泊酚。     

异丙酚靶控输注复合小剂量咪唑安定用于全麻诱导的临床观察

目的观察不同剂量丙泊酚靶控输注复合小剂量咪唑安定用于全麻诱导对心血管反应的影响,探讨两药联合应用时最适合剂量。方法40例ASAⅠ-Ⅱ级患者随机分为两组,每组20例,Ⅰ组予异丙酚靶控输注,Ⅱ组予异丙酚靶控输注,并联合应用咪唑安定0．03mg／kg;每组又随机分为A、B两个亚组各10例,A亚组丙泊酚血浆靶浓度为2μg／ml,B亚组为3μg／ml。结果ⅠA组各时点HR、SBP和DBP显著高于其余三组（P〈0．05）,且较基础值升高（P〈0．05）;ⅠB、ⅡA组HR在T0较基础值升高,其余时点低于基础值（P〈0．05）,SBP、DBP在各时点均较基础值降低（P〈0．05）;ⅡB组HR、SBP、DBP在各时点较基础值降低（P〈0．05）且低于其余三组;患者OAA／S评分达1分（BIS值55～65之间）所需时问ⅡA组较IA组、ⅡB组较IB组显著缩短（P〈0．05）;ⅡA与IA,ⅡB与IB低血压发生率无显著差异（P〉0．05）。结论咪唑安定0．04mg／kg可减少诱导所需丙泊酚血浆靶浓度至2。3μg／ml,缩短诱导所需时问．且不增加诱导过程低血压发生率。     

丙泊酚在ICU老年患者创伤后精神障碍中的应用

目的探讨丙泊酚治疗ICU老年患者创伤后精神障碍的疗效。方法50例老年创伤精神障碍患者,年龄70-90岁。随机均分为丙泊酚组（A组）和咪唑安定组（B组）,分别应用微量泵持续输注丙泊酚0．5mg·kg^-1·h^-1和咪唑安定0．04mg·kg^-1·h^-1治疗12h,比较两组Ramsay评分和治疗有效率,同时记录药物起效时间和停药后清醒时间,并监测用药前后的ECG、MAP、HR、SpO2和RR。结果A组达到Ramsay评分Ⅴ级（23例）明显多于B组（9例）（P〈0．01）。精神症状改善者,A组为24例（有效率为96％）,B组为18例（有效率为72％）,治疗效果A组明显好于B组（P〈0．01）。起效时间和清醒时间,两组相比差异有统计学意义（P〈0．01）。两组用药后MAP、HR和RR比用药前明显下降（P〈0．05）,组间比较差异无统计学意义。结论丙泊酚可能是减轻ICU老年创伤精神障碍的一种有效方法。     

应用PET研究咪唑安定对沙土鼠脑缺血／再灌注损伤的保护作用

目的：探讨正电子发射断层显像（PET）在咪唑安定对沙土鼠脑缺血／再灌注（I／R）损伤研究中的应用价值,并为咪唑安定的临床合理应用提供实验依据。方法：健康清洁级雄性蒙古沙土鼠108只,随机分为假手术组（n=36）、I／R损伤组（n=36）和咪唑安定治疗组（治疗组,n=36）。采用双血管法建立沙土鼠全脑I／R模型,假手术组仅游离双侧颈总动脉但不夹闭;I／R损伤组夹闭双侧颈总动脉10min,松开动脉夹再灌注即刻腹腔注射生理盐水50ml／kg,随后每天同一时间在动物清醒状态下腹腔注射生理盐水50ml／kg,共6d;治疗组以0．01％咪唑安定注射液5mg／kg代替生理盐水,其余处理同I／R损伤组。分别于再灌注后6h、1d、3d、7d运用PET观察脑梗死面积变化,并测定脑内丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性。结果：①脑组织再灌注面积：假手术组无明显异常,I／R损伤组与治疗组于再灌注后各时间点均较假手术组明显减小（P〈0．01）,治疗组在再灌注后6h与I／R损伤组比较差异无显著性,其余时间点均较I／R损伤组明显增加（P〈0．01）。②MDA：I／R损伤组和治疗组在各再灌注时间点MDA水平均增高,除治疗组于再灌注7d时与假手术组比较差异无显著性外,其余各时间点差异均有显著性（P〈0．01）;两组均于再灌注1d达到高峰,随后逐渐降低;治疗组于再灌注各时间点MDA水平均低于I／R损伤组（P〈0．05或P〈0．01）。③SOD：I／R损伤组和治疗组在各再灌注时间点均低于假手术组（P〈0．01）;两组均于24h降至最低,随后逐渐恢复;但治疗组再灌注1～7d均高于I／R损伤组（P〈0．01）。结论：5mg／kg咪唑安定可减少沙土鼠脑I／R损伤后脑梗死的体积,对缺血缺氧脑损伤产生了一定的保护作用;PET可完全满足小动物显像的要求。     

术前口服美托洛尔对阿托品正性心率作用的影响

目的本研究探讨术前口服美托洛尔对丙泊酚麻醉时阿托品正性心率作用的影响。方法选择择期手术的全麻病人（ASAⅠ-Ⅱ）40例,随机分成两组,每组20例,第一组为实验组（M组）,术前口服美托洛尔50mg,第二组为对照组（C组）给予安慰剂;麻醉诱导后以5mg·kg^-1·h^-1的恒速灌注丙泊酚维持麻醉,待血流动力学稳定后静注阿托品,每次5μg/kg,每次静注间隔2min,记录病人心率变化,直至病人心率升高达20bpm,阿托品总量限制在30μg/kg。结果实验组病人阿托品用量5μg/kg对心率没有明显变化,10μg/kg升高6bpm±5bpm;对照组用量在5μg/kg和10μg/kg,心率分别升高3bpm±5bpm和12bpm±6bpm,不同剂量组间差异存在统计学意义（P〈0．05）。阿托品用量达到15μg/kg,对照组63％病人心率升高达到20bpm,实验组21％病人心率升高达到20bpm,组间差异存在统计学意义（P〈0．05）。阿托品剂量达到30μg/kg,对照组90％和实验组79％病人心率升高达到20bpm,组间没有统计学差异（P〉0．05）。结论术前口服美托洛尔50mg减弱阿托品正性心率作用,该作用能够被大剂量阿托品有效逆转。     

婴幼儿直肠灌注氯胺酮-咪唑安定-阿托品混合液术前用药的评价

目的评价婴幼儿术前直肠灌注氯胺酮混和咪唑安定、阿托品的可行性。方法106例择期手术患儿，年龄2个月～2岁，随机分为3组：M组（n=39）术前直肠灌注咪唑安定0.5mg/kg、阿托品0．02mg／kg；MK组（n=34）在M组基础上加用氯胺酮4mg／kg；MKK组（n=33）在M组基础上加用氯胺酮8mg／kg。于用药前、用药后15min、与父母分离时、进入手术室时，对患儿进行镇静评分并记录用药期间副反应的发生情况。结果MK组和MKK组用药后各时点镇静评分均高于M组（P〈0．05）。与父母分离及进入手术室时，MK组与MKK组患儿熟睡率高于M组（P〈0．05）；MKK组静脉穿刺时患儿安静率为63％，高于MK组（32％）和M组（18％）（P〈0．05）。结论婴幼儿术前直肠灌注氯胺酮混合咪唑安定、阿托品安全、有效，效果优于单用咪唑安定。     

咪唑安定联合芬太尼在结肠镜检查中的应用研究

目的观察咪唑安定联合芬太尼在结肠镜检查中的镇静、镇痛效果。方法将需行结肠镜检查的145例ASAⅠ～Ⅱ级患者随机分为A组（70例）和B组（75例）。A组采用传统结肠镜方法检查并施行常规护理；B组采用无痛检查方法，即静脉推注咪唑安定0．05mg／kg、芬太尼1μg／kg，1～2min后开始进行结肠镜检查；检查前、中、后均施予针对性护理支持。结果两组MAP、HR组间变化差异有显著性意义（均P〈0．01）；B组呼吸抑制发生率为4．00％；B组92．00％患者镇静程度达Ramsay 2～3级水平，效果显著优于A组（P〈0．01）；B组镇静镇痛效果、遗忘及满意程度和再次接受结肠镜意愿显著优于A组（均P〈0．01）。结论咪唑安定联合芬太尼用于结肠镜检查具有良好的镇静、镇痛效果，且安全；护理支持是顺利完成检查的有效保障。     

雷米芬太尼和丙泊酚在小儿结肠镜检查中的临床应用

为观察雷米芬太尼和丙泊酚在小儿结肠镜检查中的应用,将60例ASAⅠ～Ⅱ级行结肠镜检查的小儿随机分为A、B、C3组,每组20例。A组静脉缓注2mg／kg的丙泊酚;B组静脉缓注雷米芬太尼0．6μg／kg后1min静脉缓注1．8mg／kg的丙泊酚;C组静脉缓注雷米芬太尼0．6μg／kg后1min静脉缓注1．8mg／kg的丙泊酚;分别记录术前、术中、术后2min的血压（BP）、心率（HR）、脉搏血氧饱和度（SPO2）、麻醉药用量、苏醒时间、检查时间和不良反应。结果显示,各组术前、术中、术后2min的BP、HR、SPO2变化无差异（P〉0．05）。C组丙泊酚用量（68．8±24．3）mg低于B组（92．8±23．1）mg及A组（109．8±43．3）mg（P〈0．05）,术后C组的苏醒时间（2．1±1．3）min少于B组（3．8±2．3）min及A组（12．8±5．6）min（P〈0．05）。结果表明,雷米芬太尼和丙泊酚联合应用,使患儿在结肠镜检查中无痛苦,安全、舒适。     

Inhalation induction

OBJECTIVES: To clarify how pharmacokinetics explains the speed and quality of mask induction with sevoflurane alone or associated with adjuvants. To describe the various techniques to obtain adequate anaesthesia for laryngeal mask or tracheal tube insertion. To give the indications, contra-indications and complications of this technique. DATA SOURCES: Data were obtained from Medline and authors clinical experience. DATA SYNTHESIS: Inhalation induction in adults affords rapid loss of consciousness similar to the intravenous route if high concentrations of sevoflurane are delivered to the patient. Time of laryngeal mask or tracheal tube insertion is longer but may be reduced by adding N(2)O and/or a low opioid dose. The interest of benzodiazepine as premedication is not established but is highly probable when considering its potentiating effect on halogenated agents. Without any adjuvant, inhalation induction maintains spontaneous ventilation better than propofol. This justifies favouring this technique when difficult intubation is anticipated. This technique is associated to less or similar cardiovascular effects than intravenous propofol. However, some patients exhibit dramatic tachycardia and arterial pressure increase that should lead to caution in cardiovascular disabled patients. This sympathetic hyperactivity occurs with epileptiform EEG activity that was never associated with postanaesthesia mental dysfunction. In aged or cardiac patients, by reducing sevoflurane concentrations from 8% to 2% (or by 2% decreasing steps), the cardiovascular effect of this inhalation induction is better than propofol. This technique is contra-indicated in HMS susceptible patients and those suffering from a myopathy, or patients with intracranial hypertension, a full stomach or active gastro-oesophageal reflux. CONCLUSION: Inhalation induction in adults remains little used in common clinical practice. Technical improvement by adding opioids and education of anesthetists should increase the diffusion of this alternative method to intravenous induction of anaesthesia.     

Ultrarapid induction

We report 250 rapid induction anesthesias performed for the purpose of preventing regurgitation and vomiting in patients with full stomach. The anesthetic technique includes administration of morphine 20 mg and droperidol 5 mg intravenously 10-15 minutes before induction, a voluntary air hyperventilation at the anesthetist's command, during which induction drugs are introduced and an induction with a mixture containing suxamethonium 2 mg/kg and thiopentone 1.4 mg/kg, administered within 1-2 seconds. Eighteen seconds after the onset of injection the loss of lid reflex is observed followed 7 seconds later by masseter muscle relaxation. Within the following 5-10 seconds intubation is carried out in full fasciculation process, before cardia relaxation. With this technique, a mean intubation time of 35 seconds is achieved. The interval of maximum regurgitation risk is lowered to 15 seconds, so that ventilation by mask and cricoid pressure are no more necessary. The technique is indicated in the young and vigorous adult and contraindicated in the old and tainted patient, in coronary patients, in those with low heart output and slowing of circulation.     

Osteoid induction

Osteoinduction is a biological principle. The implantation of tissue with inductive properties results in the proliferation and differentiation of undifferentiated cells to cartilage and bone. This process, which is similar to a cascade-type mechanism, is controlled by a series of humoral and local growth factors. It was possible to isolate a number of macromolecular substances with osteoinductive, mitogenic, or chemotactic properties specifically from the extracellular bone matrix. A deeper understanding of the regulative mechanisms as well as the greater availability of growth factors may lead to new therapeutic approaches in bone surgery.     

The impact of fluid optimisation before induction of anaesthesia on hypotension after induction

Intra-operative hypotension is a known predictor of adverse events and poor outcomes following major surgery. Hypotension often occurs on induction of anaesthesia, typically attributed to hypovolaemia and the haemodynamic effects of anaesthetic agents. We assessed the efficacy of fluid optimisation for reducing the incidence of hypotension on induction of anaesthesia. This prospective trial enrolled 283 patients undergoing radical cystectomy and randomly allocated them to goal-directed fluid therapy (n = 142) or standard fluid therapy (n = 141). Goal-directed fluid therapy patients received fluid optimisation based on stroke volume response to passive leg raise before induction; those with positive passive leg raise received intravenous crystalloid fluid boluses until stroke volume was optimised. Baseline mean arterial pressure was measured on the morning of surgery and on arriving in the operating theatre. This post-hoc analysis defined haemodynamic instability as either a > 30% relative drop in mean arterial pressure compared with baseline or absolute mean arterial pressure < 55 mmHg, within 15 min of induction. Forty-two (30%) goal-directed fluid therapy patients underwent fluid optimisation after finding an intravascular fluid deficit via passive leg raise testing; 106 (75%) goal-directed fluid therapy and 112 (79%) standard fluid therapy patients met criteria for haemodynamic instability. There was no significant difference in the incidence of haemodynamic instability between the goal-directed fluid therapy and standard fluid therapy groups using absolute mean arterial pressure drop below 55 mmHg (p = 0.58) or using pre-surgical testing or pre-surgical mean arterial pressure values as baseline (p = 0.21, p = 0.89, respectively); however, the difference in the incidence of haemodynamic instability was significant using the operating theatre baseline mean arterial pressure (p = 0.004). We conclude that fluid optimisation before induction of general anaesthesia did not significantly impact haemodynamic instability.