舒芬太尼对去甲肾上腺素诱发自发性高血压大鼠离体胸主动脉收缩的影响

Objective To investigate the effect of sufentanil on norepinephrine (NE)-induced contraction of thoracic aorta isolated from rats with spontaneous hypertension (SH) .Methods Eight male rats with SH weighing 250-300 g were used in this study. The rats were decapitated and their thoracic aortas were isolated and cut into rings 2-3 mm in length. The aorta rings were suspended for isometric tension recording. The aortic rings obtained from SH rats were divided into 4 groups ( n = 8 each) : control group and 3 sufentanil groups. The contraction of aortic rings in response to NE in the absence (control) and presence of 3 concentrations of sufentanil 7 × 10-11 ,2 × 10-10 and 1 × 10-9 mol/L was recorded. Results The amplitude of NE-induced contraction of thoracic aorta was significantly greater in 3 sufentanil groups than in control group. Sufentanil significantly inhibited the NE-induced aortic contration in proportion to concentration. Conclusion Sufentanil can inhibit NE-induced contraction of thoracic aorta isolated from rats with SH in a concentration-dependent manner.     

舒芬太尼对去甲肾上腺素诱发自发性高血压大鼠离体胸主动脉收缩的影响

Objective To investigate the effect of sufentanil on norepinephrine (NE)-induced contraction of thoracic aorta isolated from rats with spontaneous hypertension (SH) .Methods Eight male rats with SH weighing 250-300 g were used in this study. The rats were decapitated and their thoracic aortas were isolated and cut into rings 2-3 mm in length. The aorta rings were suspended for isometric tension recording. The aortic rings obtained from SH rats were divided into 4 groups ( n = 8 each) : control group and 3 sufentanil groups. The contraction of aortic rings in response to NE in the absence (control) and presence of 3 concentrations of sufentanil 7 × 10-11 ,2 × 10-10 and 1 × 10-9 mol/L was recorded. Results The amplitude of NE-induced contraction of thoracic aorta was significantly greater in 3 sufentanil groups than in control group. Sufentanil significantly inhibited the NE-induced aortic contration in proportion to concentration. Conclusion Sufentanil can inhibit NE-induced contraction of thoracic aorta isolated from rats with SH in a concentration-dependent manner.     

舒芬太尼复合艾司洛尔对全麻患者气管插管时心血管反应的影响

目的评价舒芬太尼复合艾司洛尔对全麻患者气管插管时心血管反应的影响。方法择期上腹部手术患者60例,年龄26～50岁,体重48～75kg,ASAⅠ或Ⅱ级,随机分为3组（n=20）：舒芬太尼0.5μg/ks组（Ⅰ组）、芬太尼5μg/kg＋艾司洛尔1 mg/kg组（Ⅱ组）和舒芬太尼0.5μg/kg＋艾司洛尔1 mg/kg组（Ⅲ组）。3组均静脉注射试验用药、异丙酚1.5 mg/kg和维库溴铵0.1 mg/kg麻醉诱导后气管插管,机械通气。分别于麻醉诱导前（T1）、麻醉诱导后1min（T2）、气管插管后即刻（T3）、气管插管后1 min（T4）、3min（T5）及10min（T6）记录HR,收缩压（SP）、舒张压（DP）,并于T1、T2、T4时采集桡动脉血7 ml,测定血浆肾上腺素（Ad）和去甲肾上腺素（NA）的浓度。结果与Ⅰ组比较,Ⅱ组和Ⅲ组HR、SP、DP及血浆Ad和NA的浓度降低（P〈0.05）;与Ⅱ组比较,Ⅲ组HR、SP、DP降低（P〈0.05）。与T1比较,T2时3组HR、SP、DP及血浆Ad和NA浓度降低（P〈0.05）,Ⅰ组T3时HR、SP、DP升高,T4时HR升高,Ⅱ组、Ⅲ组差异无统计学意义（P〉0.05）。结论舒芬太尼0.5μg/kg复合艾司洛尔1mg/kg可更好地预防全麻患者气管插管时的心血管反应。     

麻醉诱导前主动咳嗽对舒芬太尼诱发呛咳反应的影响

目的 观察麻醉诱导前主动咳嗽对舒芬太尼诱发呛咳反应的影响.方法 拟在全麻下行妇科手术患者400例,年龄18～65岁,随机均分为两组.主动咳嗽组(A组)诱导前嘱患者屏气后用力咳嗽2声,对照组(C组)诱导前正常平静呼吸,麻醉诱导均采用舒芬太尼0.5 μg/kg经前臂静脉给药,注射时间3s.记录舒芬太尼注射后1min内的呛咳反应,并根据呛咳次数进行严重程度分级.结果 A、C两组呛咳发生率分别为36％和39％,组间差异无统计学意义.两组总的呛咳发生率为37.5％.A组重度呛咳发生率明显低于C组(7％ vs.14％,P＜0.05).结论 诱导前主动咳嗽并不能明显降低舒芬太尼诱导的呛咳反应发生率,但可以降低呛咳严重程度.     

胸科手术后舒芬太尼静脉镇痛的剂量探讨

目的探讨普胸外科手术后舒芬太尼静脉镇痛的合理剂量和效果。方法80例普胸外科手术后的病人均分为四组,A组（芬太尼30μg／h）,B组（舒芬太尼3μg／h）,C组（舒芬太尼4μg／h）,D组（舒芬太尼5μg／h）。观察术后4、8、16、24、48h的疼痛、镇静、情绪、睡眠质量评分,并记录有无恶心、呕吐、呼吸抑制、皮肤瘙痒等不良反应,记录镇痛泵输注情况、（实际／有效）按压次数,计算单位时间实际用药量。结果四组间镇静、睡眠质量评分以及不良反应差异无统计学意义,D组疼痛评分显著低于其他三组（P〈0．05）,PCA泵按压次数最少,B、C、D组单位时间实际药量大致相近。结论普胸外科手术后舒芬太尼静脉镇痛的最佳剂量为5μg／h,且恒速背景输注比反复追加给药更容易为病人所接受。     

P物质对去甲肾上腺素诱发大鼠离体心脏功能变化的影响

目的 探讨P物质(SP)对去甲肾上腺素(NE)诱发大鼠离体心脏功能变化的影响.方法 健康成年雄性SD大鼠54只,体重250～280 g,随机分为9组:对照组(C组,n=6);10-6mol/L SP组(SP1组,n=6);10-7mol/L SP组(SB组,n=6);10-8mol/L SP组(SP3组,n=6);10-5mol/L NE组(NE1组,n=6);10-6mol/L NE组(NE2组,n=6);10-7mol/L NE组(NE3组,n=6);10-8mol/L SP+10-5mol/L NE组(SN组,n=6);10-7 mol/L NK-I受体拮抗剂+10-8 mol/L SP+10-5mol/L NE组(DSN组,n=6).分离大鼠心脏,采用Langendorff装置灌流离体心脏,记录给药后10 min内的左室收缩压(LVSP)、左室舒张末期压(LVEDP)、左室发展压(LVDP)和心率(HR),计算各指标变化率.结果 与C组比较,NE1组、NE2组和NE3组LVDP、LVSP和HR的变化率均升高,NE1组升高最明显,NE1组LVEDP变化率明显降低(P<0.05);与NE1组比较,SN组LVDP和LVSP变化率升高、HR变化率降低(P<0.05);与SN组比较,DSN组LCDP和LVSP的变化率降低(P<0.05);与NE1组比较,DSN组HR变化率降低(P<0.05).结论 10-7～10-5mol/L NE对心脏可产生明显正性变时变力作用,10-8～10-6mol/L SP对心脏无直接作用,但可增强NE的正性变力作用,抑制NE的正性变时作用;其机制可能与NK-1受体激活有关.     

腹腔注射舒芬太尼对SD大鼠气道反应性的影响

目的:观察腹腔注射舒芬太尼对SD大鼠气道反应性的影响。方法:将32只雄性SD大鼠按随机数字表法分为4组,正常对照为A组( n＝8,腹腔注射生理盐水,3 ml);实验组,B1组( n＝8,腹腔注射舒芬太尼60 μg/kg,3 ml)、B2组( n＝8,腹腔注射舒芬太尼90 μg/kg,...     

体外循环回路对预充液舒芬太尼浓度的影响

目的 评价体外循环回路对预充液舒芬太尼浓度的影响.方法 实验分为2组(n=6):西京90型大号鼓泡式氧合器体外循环回路组(A组)和玻璃容器组(B组).将预充液(琥珀酰明胶液1000ml和乳酸钠林格氏液1000 ml)预充入大号鼓泡式氧合器体外循环装置或玻璃容器中,从静脉贮血器的静脉端或玻璃容器口快速加入舒芬太尼15μg(浓度为7.5 ng/ml).在加药后3、5、10、20、30、40、50、60、70、80、90 min时,从静脉贮血器的动脉端或玻璃容器中抽取预充液1 ml,采用气相色谱质谱法检测舒芬太尼浓度.结果 与B组比较,A组各时点预充液舒芬太尼浓度明显降低(P＜0.05).结论 体外循环回路对预充液舒芬太尼有明显吸附作用.     

不同体外循环回路对预充液舒芬太尼浓度的影响

目的 评价不同体外循环回路对预充液舒芬太尼浓度的影响.方法 实验分为3组(n=6):西京90型大号鼓泡式氧合器体外循环回路组(Ⅰ组)、Termo Capiox SX18成人膜式氧合器体外循环回路组(Ⅱ组)和玻璃容器组(Ⅲ组).将预充液(琥珀酰明胶液1000 ml和乳酸钠林格氏液1000ml)预充入大号鼓泡式氧合器、膜式氧合器体外循环装置或玻璃容器中,从静脉贮血器的静脉端或玻璃容器口快速加入舒芬太尼15μg(浓度为7.5 ng/ml).于注入舒芬太尼后1、3、5、10、20、30、40、50、60、70、80、90 min时,从静脉贮血器的动脉端或玻璃容器中抽取预充液1 ml,采用气相色谱质谱法检测舒芬太尼的浓度.结果 与Ⅲ组比较,Ⅰ组和Ⅱ组各时点预充液舒芬太尼浓度降低(P＜0.05);与Ⅱ组比较,Ⅰ组各时点预充液舒芬太尼浓度降低(P＜0.05).结论 西京90型大号鼓泡式氧合器和TermoCapiox SX18成人膜式氧合器体外循环回路对舒芬太尼均有吸附作用,且前者吸附作用强于后者.     

酒石酸布托啡诺对舒芬太尼诱发咳嗽反射的影响

目的观察酒石酸布托啡诺对舒芬太尼诱发咳嗽反射的影响。 方法择期行腹腔镜胆囊切除术患者82例,ASAⅠ或Ⅱ级,随机分为两组,分别于麻醉诱导前静注以生理盐水稀释至5 ml的酒石酸布托啡诺1 mg (试验组)或生理盐水5 ml(对照组),5 min后在3 s内静注舒芬太尼0.3 μg/kg,观察并记录两组患者2 min内咳嗽反射的发生率和强度。 结果试验组患者咳嗽反射的发生率、强度明显低于对照组。 结论酒石酸布托啡诺1 mg可以抑制舒芬太尼诱发的咳嗽反射。     

右美托咪啶对原发性高血压病人术后舒芬太尼自控静脉镇痛效果的影响

目的 探讨右美托咪啶对原发性高血压病人术后舒芬太尼自控静脉镇痛效果的影响.方法 择期拟行经腹子宫全切术的原发性高血压病人60例,年龄42～63岁,体重48～72 kG,高血压分级Ⅰ或Ⅱ级,ASA分级Ⅱ或Ⅲ级,采用随机数字表法,将病人随机分为3组(n=20):对照组(C组)、不同剂量右美托咪啶组(D1组和D2组).术后24 h内行舒芬太尼PCIA,舒芬太尼100μg+托烷司琼5 mg+生理盐水100ml,背景输注速率2 ml/h,PCIA剂量0.5ml,锁定时间15 min.D1组和D2组在PCIA同时分别以0.2和0.3μg·kg-1·h-1的速率静脉输注右美托咪啶,C组在PCIA同时以0.1 ml·kg-1 的速率静脉输注生理盐水.术后24h内记录总按压次数、舒芬太尼用量和硝苯地平、麻黄碱的使用情况及呼吸抑制和呕吐的发生情况,术后24h时行Ramsay镇静评分.结果 与C组比较,D1组和D2组PCIA总按压次数减少,舒芬太尼用量降低,Ramsay镇静评分升高,硝苯地平使用率、呼吸抑制和呕吐发生率降低,D2组麻黄碱使用率升高(P＜0.05);与D1组比较,D2组PCIA总按压次数减少,舒芬太尼用量降低,Ramsay镇静评分升高,麻黄碱使用率升高(P＜0.05).结论 右美托咪啶不仅可减少原发性高血压病人术后舒芬太尼PCIA的用量,还可预防术后高血压进一步恶化.

Abstract：

Objective To investigate the effect of dexmedetomidine on postoperative patient-controlled intravenous analgesia (PCIA) with sufentanil in patients with essential hypertension. Methods Sixty ASA Ⅱ or Ⅲ patients with essential hypertension aged 42-63 yr weighing 48-72 kg undergoing hysterectomy were randomly divided into 3 groups ( n = 20 each): control group ( group C) and different doses of dexrmedetomidine groups ( group D1.2 ). PCIA was performed with sufentanil 1 μg/ml + tropisetron 5 μg/ml in 100 ml of normal saline within 24 h after operation (background infusion at 2 ml/h with a bolus dose of 0.5 ml and a 15 min lockout interval). Dexmein group C. Ramsay score was recorded. The number of attempts, consumption of sufentanil, the number of patients who needed nifedipine or ephedrine and side effects such as vomiting and respiratory depression were recoded within 24 h after operation. The level of sedation was evaluated with Ramsay sedation score at 24 h after operation.Results Compared with group C, the number of attempts, consumption of sufentanil, the number of patients who needed nifedipine and incidences of vomiting and respiratory depression were significantly decreased, while Ramsay score was significantly increased in D1 and D2 groups, and the number of patients who needed ephedrine was significanlly increased in group D2 ( P ＜ 0.05). The number of attempts and consumption of sufentanil were significantly decreased, and Ramsay score and the number of patients who needed ephedrine were significantly increased in group D2 compared with group D1 ( P ＜ 0.05). Conclusion Dexmedetomidine can not only reduce the consumption of sufentanil for postoperative PCIA, but also prevent postoperative hypertension from deteriorating in patients with essential hypertension.     

异丙酚对高血压大鼠胸主动脉内皮型一氧化氮合酶和诱导型一氧化氮合酶表达的影响

目的 评价异丙酚对高血压大鼠胸主动脉内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)表达的影响.方法 SD大鼠,雌雄各半,体重240～ 280 g,采用皮下注射去氧皮质酮的方法制备高血压模型,采用随机数字表法,将64只造模成功的大鼠随机分为4组(n＝16):高血压组(H组)、小剂量异丙酚组(P1组)、中剂量异丙酚组(P2组)和大剂量异丙酚组(P3组).P1组、P2组和P3组分别静脉输注异丙酚20、30、40 mg·kg-1·h-13 h,H组给予等容量生理盐水.分别于给药前、给药1h、3h时记录平均动脉压(MAP).给药3h时处死大鼠,摘眼球法采集血样,硝酸还原酶法测定血清一氧化氮(N0)浓度,取胸主动脉,采用RT-PCR和Western blot法测定eNOS mRNA、iNOS mRNA及其蛋白表达水平.结果 与H组比较,P1组、P2组和P3组给药3h时MAP降低,血清NO浓度升高,主动脉eNOS mRNA及其蛋白表达上调,主动脉iNOS mRNA及其蛋白表达下调,且呈剂量依赖性(P<0.05或0.01).结论 异丙酚降低高血压大鼠血压的机制与下调iNOS表达,上调血管内皮细胞eNOS表达,促进NO释放有关.     

胸主动脉分支血管的CT研究

目的 利用CT血管造影测量胸主动脉分支血管,为胸主动脉腔内修复技术提供相关的血管解剖指导.方法 收集2008年1月-2012年2月在广州军区武汉总医院进行胸主动脉CT血管造影检查的739例患者资料,测量升主动脉、主动脉弓、弓上分支的直径和长度,并进行统计、分析.结果 主动脉弓分为标准型和变异型,其中标准型最常见,占总例数的91.1％,变异型占8.9％.主动脉弓标准型患者的冠状动脉开口处升主动脉直径为(35.7±4.3) mm,头臂干开口处升主动脉直径为(33.6±4.2) mm,头臂干与左颈总动脉之间的主动脉弓直径为(29.4±5.7) mm,左颈总动脉与左锁骨下动脉之间的主动脉弓直径为(27.6±4.2) mm,左锁骨下动脉开口处降主动脉直径为(25.4±4.5) mm,头臂干在主动脉弓分支处的直径为(12.9±0.9) mm,左颈总动脉在主动脉弓分支处的直径为(8.5±0.7)mm,左锁骨下动脉在主动脉弓分支处的直径为(10.4±1.1) mm,冠状动脉与头臂干之间的管壁长度为(53.3±12.5) mm,头臂干与左颈总动脉之间的管壁长度为(4.7±1.5) mm,左颈总动脉与左锁骨下动脉之间的管壁长度为(7.9±2.6)mm,头臂干起始处至右锁骨下动脉开口处长度为(41.1±8.2)mm,左锁骨下动脉起始处至椎动脉开口处管腔长度为(38.5±5.7) mm,头臂干与左颈总动脉间距的平面与矢状面之间的夹角为(71.2±7.2)°,左颈总动脉与左锁骨下动脉间距的平面与矢状面之间的夹角为(31.1±2.9)°.结论 CT测量所得的胸主动脉数据可以为血管支架的生产提供支持,还能为腔内修复术中支架的定位释放提供指导.     

脂多糖对离体大鼠胸主动脉和肺组织HO-1mRNA及蛋白表达的影响

目的 观察离体大鼠胸主动脉和肺组织脂多糖（Lipopolysaccharide,LPS)孵育后血红素氧合酶－1（HO－1）mRNA及蛋白表达时间依从性的变化。方法 24只Wistar大鼠颈椎脱臼处死，取其胸主动脉和肺组织，随机分成四组：对照组（n=6)，实验组包括LPS3、8、24组（均为n=6)，分别与LPS（1μg/ml）孵育3、8、24h。采用蛋白免疫杂交（Western blot）和半定量聚合酶链反应（RT－PCR）分别测定HO－1蛋白和mRNA表达，结果 与对照组相比，胸主动脉HO－1蛋白表达LPS3组即达最高值（P＜0．05），LPS8和LPS24组仍处于较高水平（P＜0．05）；肺组织HO－1蛋白表达LPS3组已开始升高（P＜0．05）,LPS8力LPS24组仍处于较高水平（P＜0．05）；肺组织HO－1蛋白表达LPS3组已开始升高（P＜0．05），LPS8组达最高水平（P＜0．01），LPS24组有下降趋势，但仍与对照组有差异（P＜0．05）。与对照组相比，胸主动脉HO－1mRNA表达LPS3组即达最高值（P＜0．05），LPS8组较LPS3组无明显变化（P＞0．05），而LPS24且则恢复至始水平；肺组织HO－1mRNA表达LPS3组开始升高（P＜0．05），LPS8组达到最大值（P＜0．01），LPS24组回到基础水平（P＞0．05）。结论 脂多糖可以明显促进大鼠胸主动脉和肺组织HO－1mRNA及蛋白表达，且两种组织表现出不同的时间依从性变化，可能与感染性休克体肺循环不同变化的病生理机制有关。     

Effect of temperature increase on the distensibility of porcine thoracic aorta

The objective of the study was to investigate the temperature impact on the elasticity of porcine thoracic aorta. Under general anesthesia, 16 Landrace pigs were subjected to thoracotomy, and the descending thoracic aorta was removed and stored in normal saline. Serial sections of the vessel created cylindrical aortic specimens which were tested in a uniaxial tension device to determine the elastic properties of the aortic wall. In the control, Group A (n = 8), the aortic tissues were tested while immersed in normal saline bath of temperature TA = 37.0 +/- 0.5 degrees C, while in Group B, the temperature was TB = 40.0 +/- 0.5 degrees C. Each experiment took place only after the tissues had remained for 15 min in temperature TA or TB. For the results, the stiffness modulus of Group B showed a significant decrease (P < 0.05) at medium strain level deformation (e = 1, SB1 = 114 +/- 8 Pa) as well as at high strain level deformation (e = 2, SB1 = 1182 +/- 48 Pa) in comparison with the control, Group A (e = 1, SA1 = 147 +/- 15 Pa; e = 2, SA1 = 1479 +/- 64 Pa). It is concluded that temperature increase facilitates, in vitro, the expansion of descending thoracic aorta. We assume that thermal treatment may be another means against the stiffening of aorta, which calls for further research.     

右美托咪定及其联合舒芬太尼预先给药对大鼠心肌缺血再灌注损伤的影响

目的 探讨右美托咪定及其联合舒芬太尼预先给药对大鼠心肌缺血再灌注损伤的影响.方法 健康清洁级雄性SD大鼠50只,体重250～300 g,采用阻断左冠状动脉前降支30 min再灌注120 min的方法制备心肌缺血再灌注模型.采用随机数字表法,将大鼠分为5组(n=10):假手术组(S组)只穿线,不结扎左冠状动脉前降支;缺血再灌注损伤组(IR组);右美托咪定预先给药组(DP组)腹腔注射右美托咪定5 μg/kg,30 min后制备模型;舒芬太尼预先给药组(SP组)腹腔注射舒芬太尼10μg/kg,30 min后制备模型;右美托咪定+舒芬太尼预先给药组(DS组)腹腔注射右美托咪定5 μg/kg和舒芬太尼10 tμg/kg,30 min后制备模型.再灌注120 min时,取血样,测定血清CK、LDH浓度;处死大鼠,观察心肌组织病理学结果,计算心肌梗死体积,测定心肌组织MDA含量及SOD活性.结果 与S组相比,其余各组血清CK、LDH浓度升高,心肌梗死体积增加,心肌SOD活性降低,IR组、DP组和SP组心肌MDA含量升高(P＜0.05或0.01),DS组心肌MDA含量差异无统计学意义(P＞0.05);与IR组相比,DP组、SP组和DS组血清CK和LDH浓度、心肌MDA含量降低,心肌梗死体积减少,心肌SOD活性升高(P＜0.05);与DS组相比,DP组和SP组血清CK浓度升高,心肌梗死体积增加,心肌MDA含量升高(P＜0.05),DP组血清LDH浓度升高和心肌SOD活性降低(P＜0.05).DS组心肌病理学损伤较DP组和SP组减轻.结论 右美托咪定预先给药可减轻大鼠心肌缺血再灌注损伤,其联合舒芬太尼预先给药时该效应强于两者单独应用,机制与增强抗氧化能力、抑制脂质过氧化反应有关.