丙泊酚复合麻醉在实验犬外科手术中的效果观察

目的丙泊酚复合麻醉应用于实验犬外科手术,进行效果评价。方法成年健康杂种犬13只,雌雄不限。术前30 min肌内注射阿托品0.5 mg,吗啡10 mg,进行气管插管,静脉注射氯胺酮50 mg,静脉注射丙泊酚首次剂量5 mg/kg体重,维持剂量1 mg/kg。结果丙泊酚复合麻醉,平均麻醉起效时间40 s,首次剂量平均维持17.3min,重复给药平均维持13.6 min,无死亡。丙泊酚有较强的麻醉效果,诱导时间短,起效快,恢复快速平稳,而且无副作用。结论丙泊酚复合麻醉适合于犬的外科手术实验,是一种较为理想的麻醉方法。     

小剂量利多卡因在无痛宫腔镜术中的应用

目的：观察静注利多卡因在无痛宫腔镜术的应用效果。方法：120例择期宫腔镜手术患者,随机均分为L、C两组。L组麻醉诱导前缓慢静脉推注利多卡因1mg／kg;C组以生理盐水替代。两组均静注丙泊酚1—1．5mg／kg进行麻醉诱导至睫毛反射消失,术中酌情追加丙泊酚。麻醉开始后,询问患者是否有静脉注射痛,观察记录术中及术后疼痛情况。结果：两组术中血压、心率平稳。L组较C组丙泊酚注射痛及术中术后疼痛程度减轻（P〈0．05）。结论：利多卡因复合丙泊酚用于无痛宫腔镜不良反应小,有利于病人术后恢复。     

氯胺酮加丙泊酚与芬太尼加丙泊酚用于学龄前 小儿非心脏手术的麻醉效果比较

目的:比较芬太尼加丙泊酚与氯胺酮加丙泊酚用于学龄前小儿非心脏手术的麻醉效果。方法:患儿70例,随机分为两组,F组(n=35),用芬太尼2-3 ug／kg,阿曲库铵0．5 mg／kg,丙泊2-3 mg／kg,静脉注射诱导插管,然后微泵持续注射芬太尼0．03-0．06 ug/kg．min-1,阿曲库铵4-8 ug/kg．min-1,丙泊酚80-150 ug／kg．min-1,K组(n=35),用氯胺酮1-1．5 mg／kg,阿曲库铵0．5 mg/kg,丙泊酚2-3 mg／kg,静脉注射诱导插管,然后微泵持续注射氯胺酮30-60 ug／kg．min-1,阿曲库铵与丙泊酚用量同F组,根据术中的情况予以调整。分别记录两组病例在用药前后的收缩压(SBP)、舒张压(DBP)、心率(HR)、麻醉效果、停药至导管拔除时间,以及拔管后因气道梗阻再次插管等情况。结果:K组病例在麻醉诱导时循环稳定,拔管后无呼吸抑制的发生,但术毕拔管的时间延长,F组病例麻醉诱导时HR、SBP、DBP降低明显,拔管后有3例气管痉挛致呼吸抑制重新插管。结论:氯胺酮复合丙泊酚用于学龄前小儿非心脏手术的麻醉,麻醉效果确切,可控性强,麻醉诱导平稳,术中易于调整,术毕拔管虽时间略为延长,但可避免呼吸抑制的发生,较为安全。     

小型猪生物可降解支架置入术中不同麻醉方法的研究

目的比较两种不同麻醉方法对小型猪的麻醉效果。方法将12头小型猪随机分成两组,每组6头,一组是戊巴比妥钠复合氯胺酮静脉麻醉（Ⅰ组）,另一组是丙泊酚复合氯胺酮静脉麻醉（Ⅱ组）。麻醉后对动物实施心脏生物可降解支架置入术,观察动物麻醉起效时间、苏醒时间、麻醉效果、呼吸频率（RR）、心率（HR）、血氧饱和度（SpO2）及术后苏醒情况。结果两种方法麻醉后,动物分别在7.6±2.4 min（Ⅰ组）、2.4±1.4 min（Ⅱ组）进入麻醉状态（P〈0.05）。术后苏醒时间分别为30.8±8.8 min（Ⅰ组）、16.5±2.8min（Ⅱ组）（P〈0.05）,Ⅱ组动物比Ⅰ组动物苏醒平稳（P〈0.05）。两组心率及呼吸频率变化无明显差别,而氧饱和度在第10 min（Ⅰ组87%,Ⅱ组92%）和30 min（Ⅰ组94%,Ⅱ组89%）由于追加麻醉药后,两组值差异较大,但很快恢复正常。Ⅱ组麻醉效果较Ⅰ组麻醉效果好。结论两种麻醉方法均能达到良好的麻醉效果,丙泊酚复合氯胺酮麻醉较戊巴比妥钠复合氯胺酮麻醉的效果强且术后苏醒快,是一种比较理想的麻醉方法。     

小剂量利多卡因在无痛宫腔镜术中的应用

目的:观察静注利多卡因在无痛宫腔镜术的应用效果。方法:120例择期宫腔镜手术患者,随机均分为L、C两组。L组麻醉诱导前缓慢静脉推注利多卡因1 mg/kg;C组以生理盐水替代。两组均静注丙泊酚1-1.5mg/kg进行麻醉诱导至睫毛反射消失,术中酌情追加丙泊酚。麻醉开始后,询问患者是否有静脉注射痛,观察记录术中及术后疼痛情况。结果:两组术中血压、心率平稳。L组较C组丙泊酚注射痛及术中术后疼痛程度减轻(P<0.05)。结论:利多卡因复合丙泊酚用于无痛宫腔镜不良反应小,有利于病人术后恢复。     

山羊单纯与复合全身麻醉效果的比较

目的对比山羊单纯麻醉与复合麻醉的效果,探讨一种安全高效便捷的山羊麻醉方法。方法选取山羊30只,随机分为A、B、C三组,A组给予单纯戊巴比妥钠麻醉,B组给予单纯氯胺酮麻醉,C组给予地西泮、戊巴比妥钠和氯胺酮复合麻醉,记录三种麻醉方法的起效时间、麻醉维持时间、麻醉药物用量及麻醉死亡率。结果地西泮、戊巴比妥钠和氯胺酮复合麻醉,起效快、麻醉维持时间长、动物死亡率低、麻醉效果好。结论安定、戊巴比妥钠和氯胺酮复合麻醉优于单纯麻醉,是一种高效、便捷、安全山羊全身麻醉方法。     

不同注药方法对丙泊酚注射痛的影响

目的:比较不同注射部位对丙泊酚注射痛的影响.方法:选择ASA Ⅰ-Ⅱ自愿接受无痛人工流产手术患者200例,随机分为4组,(n=50).Ⅰ组手背静脉推注丙泊酚;Ⅱ组肘部静脉推注丙泊酚;Ⅲ组肘部推注20mg 2%利多卡因后即刻静脉推注丙泊酚;Ⅳ组手背推注20mg 2%利多卡因后即刻静脉推注丙泊酚.记录各组患者的疼痛分级评分.结果:Ⅱ组与Ⅳ组比较丙泊酚注射痛无差异;Ⅱ组与Ⅲ组比较丙泊酚注射痛无差异;Ⅱ组与Ⅳ组比较发生丙泊酚注射痛的程度轻.结论:选择肘部静脉静推丙泊酚且无需预推利多卡因注射痛最轻.     

丙泊酚与咪哒唑仑复合氯胺酮用于小儿心导管术麻醉效果研究

目的:探讨丙泊酚与咪哒唑仑复合氯胺酮用于小儿心导管术麻醉的优缺点与安全性。方法:将2008年7月~2012年7月入住我院的100例行心导管术的先心病患儿按照抽签法随机地均分为A、B组,A组采用6 mg/(kg·h)丙泊酚+3 mg/(kg·h)氯胺酮维持,B组采用0.15 mg/(kg·h)咪达唑仑+3 mg/(kg·h)氯胺酮维持,比较两组麻醉效果、HR、SPO2、MAP、体动次数、停药唤醒时间及不良反应发生率。结果:对照组麻醉优良率为80.00%,小于观察组(100.00%)(P0.05);两组术前MAP、HR差异无统计学意义(P0.05),但股动脉穿刺时二者差异具有统计学意义(P0.05),两组术中SPO2差异无统计学意义(P0.05),两组体动次数、停药唤醒时间相比,具有统计学差异(P0.05,P0.01);对照组不良反应发生率为24.00%,明显大于观察组(10.00%),两组相比,差异具有显著的统计学意义(P0.01)。结论:咪哒唑仑复合氯胺酮用于小儿心导管术麻醉效果显著,安全性高,值得在临床上加以推广并应用。     

丙泊酚复合蓝博刻宁对无痛人流术麻醉效果的临床观察

目的：观察丙泊酚复合蓝博刻宁对无病人流术麻醉效果的临床效果。方法：100例无病人流患者随机分为A、B两组;A组给予丙泊酚2—3mg/kg,缓慢推注。B组首先缓慢推入蓝博刻宁（氢溴酸高乌甲素）8mg,然后给予丙泊酚2—3mg/kg．术中根据需要分次推注丙泊酚以满足手术要求。结果：B组丙泊酚用量明显少于A组（P〈0．05）,其镇痛作用明显优于A组（P〈0．05）,术后宫缩痛也比A组轻（P〈0．05）。A组住院时间明显短B组（P〈0,05）。结论：丙泊酚伍用小剂量氢溴酸高鸟甲素用于人工流产较单用大剂量丙泊酚具有麻醉效果好,有着人先效减少丙泊酚用量,明显减少术后宫缩痛,缩短患者的住院时间,利于患者早日康复出院。     

小儿上肢骨折手术的快通道麻醉

目的:观察喉罩下丙泊酚复合雷米芬太尼加神经刺激器引导下臂丛阻滞的快通道麻醉在小儿上肢骨折术中的应用效果,并与传统的麻醉方法咪唑安定加氯胺酮作比较.方法:选择ASA Ⅰ级小儿上肢骨折手术40例.随机分为2组:试验组(喉罩下丙泊酚复合雷米芬太尼加神经刺激器引导下臂丛阻滞)20例和对照组(咪唑安定+氯胺酮)20例.试验组惠儿静脉注射丙泊酚和雷米芬太尼后置入喉罩,连接麻醉机控制通气,麻醉维持采用丙泊酚和雷米芬太尼持续输注.1%利多卡因8□/□在神经刺激器引导下臂丛阻滞,手术结束停麻醉药.对照组静脉给予咪唑安定和氯胺酮,术中微量泵入咪唑安定加氯胺酮,术中根据需要调整输注速度,手术结束前5min停药.记录两组患儿的镇静镇痛效果、术中SPO2、手术时间、苏醒时间.结果:两组惠儿术中镇静镇痛效果均能满足手术需要,差异无统计学意义;两组患儿术中SPO2差异有统计学意义,试验组对气道的控制优于对照组;两组患儿手术时间差异无统计学意义,苏醒时间差异有统计学意义,对照组显著长于试验组.结论:喉罩下丙泊酚复合雷米芬太尼加神经刺激器引导下臂丛阻滞是小儿上肢骨折手术一种很好的快通道麻醉技术.     

氯胺酮麻醉对乳鼠脑细胞凋亡的影响

目的探讨临床上常用的麻醉剂氯胺酮对乳鼠脑细胞凋亡的影响。方法新生7日龄SD大鼠15只,随机分成3组：氯胺酮低剂量组、高剂量组分别腹腔注射20 mg/kg、80 mg/kg氯胺酮,对照组给予等量的生理盐水。麻醉后24 h,取脑组织作HE染色,用TUNEL法检测脑细胞的凋亡情况,用免疫组织化学法检测Caspase-3的表达水平。结果与对照组比较,氯胺酮低剂量组的凋亡细胞增多但不明显（P〉0.05）,神经元核固缩和Caspase-3阳性细胞数明显增多（P〈0.05）;氯胺酮高剂量组的凋亡细胞数、神经元核固缩及Caspase-3阳性细胞数显著性增加（P〈0.05）。神经元核固缩、凋亡细胞和Caspase-3阳性细胞均以皮层区多见。结论 80 mg/kg氯胺酮可引起乳鼠脑细胞凋亡,以皮层区为主,Caspase-3的激活可能是其作用机制之一;20 mg/kg氯胺酮对乳鼠脑细胞凋亡的影响较轻微,其临床等效剂量为3 mg/kg。氯胺酮小儿麻醉用量不宜过多,避免引起脑细胞的凋亡。     

盐酸戊乙奎醚与丙泊酚联合用于无痛人工流产术的临床研究

目的:评价盐酸戊乙奎醚联合丙泊酚减轻人工流产术后疼痛的效果.方法:ASAⅠ-H级人工流产术患者100例,随机分为观察组和对照组.处理组先缓慢静脉注射盐酸戊乙奎醚注射剂1mg,30min后静脉注射丙泊酚2.5mg/kg;;对照组单独静脉注射丙泊酚2.5mg/kg.两组丙泊酚静注速率均为5mg/s.结果:处理组苏醒即刻苏醒后15min和30min宫缩痛的VAS评分分别为(3.13±0.15)、(2.02±0.11)和(0.87±0.09)分,明显低于对照组的(4.47± 0.35)、(3.54± 0.14)及(2.01±0.12)(P＜0.01).结论:盐酸戊乙奎醚联合丙泊酚镇痛能减轻人工流产术后的疼痛.     

老年手术患者应用丙泊酚复合瑞芬太尼喉罩麻醉的临床效果观察

目的：探讨靶控输注丙泊酚复合瑞芬太尼喉罩麻醉在老年手术患者中的临床应用效果,为临床麻醉提供参考。方法：选取127例老年手术患者作为研究对象,随机分为A、B、C3组,A组43例（采用瑞芬太尼复合丙泊酚麻醉,喉罩通气）、B组42例（采用丙泊酚麻醉,喉罩通气）,C组42例（采用瑞芬太尼复合丙泊酚麻醉,面罩通气）,均采用靶控输注静脉麻醉法。观察麻醉诱导时间、术中反应、麻醉效果、镇静效果评分、苏醒时间、认知功能以及不良反应发生率等指标。结果：丙泊酚总用量：A组为（335．2±56．4）mg,B组为（466．5±64．8）mg,C组为（334．8±59．7）mg,经方差分析,差异有统计学意义,F=6．513,P〈0．05;Ramsay评分：A组6分的例数为37例（86．0％）,B组为30（71．4％）,C组为34（81．0％）,经卡方检验,差异有统计学意义,X^2=5．832,P〈0．05;不良反应发生率：A组为5例（11．6％）,B组为15例（35．7％）,C组为7例（16．7％）,经卡方检验,差异有统计学意义,X^2=7．546,P〈0．05。结论：老年手术患者应用丙泊酚复合瑞芬太尼喉罩麻醉效果显著,安全有效。     

Diazepam and propofol used as anesthetics during open-heart surgery do not cause chromosomal aberrations in peripheral blood lymphocytes

Diazepam is a benzodiazepine with anticonvulsant, anxiolytic, sedative and muscle-relaxing properties. Many aspects of its toxicity have been investigated, including genotoxic and carcinogenic effects in various model systems. However, it is still unclear whether diazepam is in fact a genotoxic agent. Propofol is a rapid-onset, short-acting intravenous anesthetic agent. It is used widely for the induction and maintenance of anesthesia as well as for long-term sedation in intensive care units. There is limited information in the literature on its genotoxic effects. Both drugs are commonly used as anesthetic in patients undergoing open-heart surgery. Therefore, we investigated the possible genotoxic effects of propofol and diazepam in those patients, using a chromosomal aberration (CA) assay. Peripheral blood samples were collected from 45 patients before induction of anesthesia and at the end of the anesthesia with diazepam or propofol. In Group I (n=24), anesthesia was induced with 0.2 mg kg(-1) diazepam and 10 microg kg(-1) fentanyl. In Group II (n=21), anesthesia was induced with 1 mg kg(-1) propofol and 10 microg kg(-1) fentanyl. Pancuronium bromide (0.1 mg kg(-1)) was administered for skeletal muscle relaxation in both groups. Anesthesia was maintained by diazepam administration at 5 mg kg(-1) in Group I or by continuous propofol administration at 2-4 mg (kg h)(-1) in Group II. All patients received 0.02 mg kg(-1) pancuronium and 5 microg kg(-1) fentanyl boluses at 30-40 min intervals for anesthesia maintenance. Body temperature was controlled during bypass in the two groups. We found that the mean frequency of CAs in both groups before and at the end of the anesthesia were not statistically significantly different. Our analysis also indicated that age, smoking habit and gender were not confounding factors. In conclusion, our results indicate that diazepam and propofol do not exert genotoxic effects in blood cells during open-heart surgery.     

The effects of different anaesthetic treatments on the adreno-cortical functions and glucose levels in NZW rabbits

The effects of five anaesthetics on the corticosterone, cortisol and glucose concentrations were investigated in the NZW rabbit. Sixty animals were assigned to 6 treatment groups (n= 10 per group): control ( iv saline solution injection), ketamine (10 mg/kg iv) with either xylazine (3 mg/kg iv) or diazepam (2 mg/kg iv), pentobarbitone (30 mg/kg iv), thiopentone (20 mg/kg iv) and fentanyl/droperidol (1 mg/kg sc). Plasma glucocorticoids were measured by competitive enzymeimmunoassay EIA and glucose by an autoanalyzer, previously validated for this species in both cases. Blood samples were obtained at 6 time-points: before injection, at 10, 30, 60, 120 min and 24 h after injection of the anaesthetics/saline. A significant decrease of plasma glucocorticoids at 10-60 min was observed in the pentobarbitone and fentanyl/ droperidol groups, whereas the administration of ketamine/diazepam or thiopentone stimulated plasma glucocorticoid release, principally in the recovery period. However, in the ketamine/xylazine group no changes were observed in the glucocorticoid levels, except for a significative increase of cortisol at 60-120 min. Glucose levels significantly increased after ketamine/diazepam administration and principally, after ketamine/xylazine treatment. The present data suggest that ketamine/xylazine has little effect on glucocorticoid levels and provides an adequate level of surgical anaesthesia, hence it would be the anaesthetic of choice, although the hyperglycaemic effect after injection has to be considered for any experimental procedures in rabbits.     

Hippocampus and amygdala neurotoxicity produced by systemic lidocaine in adult rats

There is evidence that using lidocaine-treated cellular culture produces cell damage. However, there are no studies in vivo demonstrating the potential injurious effect of lidocaine on the central nervous system. Therefore, the aim of our study was to investigate if lidocaine is involved in neuronal damage in the CA3 hippocampus and amygdala regions when using a single subconvulsive or a convulsive lidocaine dose. Two-month-old male Wistar rats (57) were used. The animals were randomly assigned to one of three groups. Group I received 0.9% saline ip (n=9), group II received a single lidocaine dose of 60 mg/kg (n=18), and group III received 90 mg/kg ip (n=12). At day 2, 7, and 10 after the dosing, three to six rats per group were sacrificed. The brains of the rats were removed and were embedded in paraffin. Coronal cuts of 7 microm were made. Each brain section was stained with cresyl-eosin. We evaluated the number of normal and abnormal neurons in the hippocampal CA3 (pyramidal) and basolateral amygdala (large and medium neurons) regions in a 10,000 microm2 section. To explore an association between lidocaine-induced seizure and neuronal damage, diazepam was used (10 mg/kg ig) as an anticonvulsant two hours before a 90 mg/kg dose of lidocaine. Lidocaine causes a morphological neuronal alteration in the CA3 hippocampal region and the basolateral amygdala and possibly an inhibition-excitation imbalance. Diazepam prevents lidocaine-induced seizures, but not neuronal damage in brain structures. Interaction of lidocaine with the membrane components produces disrupted Ca+2 homeostasis and causes neuronal damage. Moreover, it is possible that lidocaine or its metabolites could actively participate in the neuronal damage observed.     

Immobilization of Himalayan tahr with a xylazine-ketamine mixture and reversal with atipamezole under field conditions

Twenty-nine free-ranging Himalayan tahr (Hemitragus jemlahicus) were darted in the Sagarmatha National Park (Nepal) using different combinations of xylazine and ketamine. Animals in Group 1 (n = 4) received a mean xylazine-ketamine dose of 2.77 +/- 0.99 mg/kg xylazine plus 3.32 +/- 0.19 mg/kg ketamine in males and 2.39 +/- 0.10 mg/kg xylazine plus 4.29 +/- 0.17 mg/kg ketamine in females. Animals in Group 2 (n = 25) received a mean xylazine-ketamine dose of 1.70 +/- 0.41 mg/kg xylazine plus 3.06 +/- 0.74 mg/kg ketamine in males and 1.82 +/- 0.29 mg/kg xylazine plus 3.29 +/- 0.52 mg/kg ketamine in females. No anesthetic-related mortality was recorded. Anesthesia was reversed by a standard dose of 11 mg/animal of atipamezole administered by intramuscular injection. Although all anesthetic dosages immobilized free-ranging tahr successfully, a quick and smooth recovery was obtained (11.1 +/- 5.6 min) only with the dosages of Group 2.