异氟醚预处理延迟相对兔心肌缺血-再灌注损伤核因子-κB的影响

目的 探讨异氟醚预处理延迟相对心肌缺血-再灌注损伤的保护机制.方法 雄性新西兰兔30只,体质量2.0～2.5 ks.随机分成3组(n=10):假手术组(C组)、缺血再灌注组(I/R组)、2.0%异氟醚预处理组(S组).C组吸入100%氧气2 h,24 h后仅行左冠脉套线而不阻断160 min,I/R组吸入100%氧气2 h,24 h后行左冠状动脉前降支阻断40 min,再灌注120 min;S组吸入2.0%异氟醚+100%氧气2 h,24 h后处理同I/R组.各组分别于左冠前降支阻断前20 min(TI)、左冠前降支阻断20 min(T2)、左冠前降支阻断40 min(T3)、心肌再灌注1 h(T4)、心肌冉灌注2 h(T5)五个时点抽取颈内动脉血ELISA法测血清IL-10和TNF-α水平.再灌注结束后观察心肌细胞超微结构的变化,免疫印记法测心肌核因子-κB(NF-κB)活性水平,同时用伊文思蓝和TTC染色法测心梗面积.计量资料采用均数±标准差(x±s)表示,用SPSS 13.0统计学软件进行分析,组间采用方差分析,以P<0.05为差异具有统计学意义.结果 与I/R组比,S组IL-10明显升高(P<0.05),TNF-α明显降低(P<0.05),NF-κB表达降低(P<0.05),心肌梗死面积减少(P<0.05).结论 异氟醚预处理延迟相通过抑制心肌NF-κB的活性,调控炎性细胞因子平衡来减轻心肌缺血-再灌注损伤发挥保护作用.     

异氟烷预处理对心脏换瓣术患者血MMP-9的影响及其对心肌的保护作用

目的:观察异氟烷预处理对体外循环(cardiopulmonary bypass,CPB)心脏换瓣术患者围术期血浆基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)及心肌超微结构的影响,评价其对心肌的保护作用.方法:择期CPB下行瓣膜置换术的心脏瓣膜病患者30例,随机分为异氟烷预处理组(异氟烷组,n＝15)和对照组(n＝15),异氟烷组在麻醉诱导后CPB前吸入1.1%～1.2%(呼气末浓度)的异氟烷30 min,洗脱15 min,对照组不吸入异氟烷,其余用药两组无区别.分别于切皮前(T0),主动脉开放30 min(T1),6 h(T2),12 h(T3)及24 h(T4)经桡动脉取血测血浆MMP-9浓度,分别于CPB前后取部分右心耳组织电镜下观察超微结构.结果:与T0比较,对照组血浆MMP-9浓度在T1-T3显著增加,异氟烷组血浆MMP-9浓度只在T1显著升高(P<0.01);与对照组比较,异氟烷组血浆MMP-9浓度在T2显著降低(P<0.01),在T1-T3各时点与T0的差值均显著降低(P<0.01).电镜下可见对照组CPB后心肌细胞损伤比异氟烷组严重.结论:异氟烷预处理能显著抑制心脏换瓣术患者CPB后MMP-9的分泌增多,这可能是其对心脏换瓣术患者心肌保护的机制之一.     

艾司洛尔对老年患者非心脏手术围麻醉期应激反应的抑制作用

目的观察静脉持续输注艾司洛尔对老年患者非心脏手术围麻醉期应激反应的抑制作用。方法65岁以上择期全麻气管插管下行非心脏手术的患者40例，随机分为艾司洛尔组（n=20）与对照组（n=20）。艾司洛尔组麻醉前先静脉注射艾司洛尔0．25mg／kg，然后以20～50μg／（kg·min）的速度用输液泵持续输注，直到气管拔管后5min；对照组以生理盐水替代。记录入室、气管插管前、气管插管后即刻、切皮、手术结束、患者睁眼及拔管后即刻HR、MBP、RPP，以及入室、插管后即刻、切皮、手术结束及拔管后血糖、血香草扁桃酸（BVMA）及血皮质醇水平。结果与对照组比较，艾司洛尔组的HR、RPP在插管后即刻、患者睁眼以及气管拔管后即刻，MBP在气管插管后及睁眼时显著降低（P〈0．05），血糖值在手术结束及拔管后显著降低（P〈0．05或P〈0．01）。艾司洛尔组的芬太尼与异丙酚总量分别为（0．4±0．1）mg和（450．8±98．2）mg，显著少于对照组的（0．5±0．1）mg与（580．3±125．7）mg（P〈0．05）。结论艾司洛尔围麻醉期持续静脉输注可以很好地控制老年患者非心脏手术的应激反应，抑制围麻醉期患者血糖的升高，减少老年患者的麻醉药用量。     

阿片受体在异氟醚延迟预处理减轻兔心肌缺血再灌注损伤中的作用

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.     

阿片受体在异氟醚延迟预处理减轻兔心肌缺血再灌注损伤中的作用

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.     

乌司它丁对油酸致急性肺损伤大鼠肺组织血红素氧化酶-1的影响

目的:探讨乌司他丁对油酸致急性肺损伤大鼠肺组织血红素氧化酶-1表达的影响.方法 30只成年SD大鼠,随机分为3组(n＝10).正常组(A组)经大鼠尾静脉注射0.2mL/kg生理盐水;急性肺损伤组(B组)、乌司他丁组(C组)经大鼠尾静脉注射油酸0.2mL/kg制成急性肺损伤模型,随后立即给予A组、B组腹腔注射生理盐水10mL/kg,C组100ku/kg的乌司他丁腹腔注射.测取动物4h时间点呼吸频率和左心室动脉血氧分压,并于4h后取右下肺组织行HE染色和HO-1免疫组织化学检查,观察光镜下病理改变以及血红素氧化酶-1的表达.结果: 乌司他丁能显著改善油酸所致急性肺损伤所致的呼吸窘迫;肺组织血红素氧化酶-1在对照组仅有少量表达,急性肺损伤组表达增多,乌司他丁干预组表达明显增强.结论:乌司他丁可通过增加肺组织中血红素氧化酶-1的表达而发挥保护作用.     

阿片受体在异氟醚延迟预处理减轻兔心肌缺血再灌注损伤中的作用

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.     

异氟醚预处理对心脏联合瓣膜置换术患者左心功能的影响

目的观察异氟醚预处理对心脏手术患者左心功能的影响。方法择期二尖瓣和主动脉瓣联合置换术患者30例,随机均分为两组:G组麻醉诱导后吸入1.1%~1.2%的异氟醚30min,洗脱15 min;C组不吸入异氟醚作为对照。于吸入异氟醚前(T0)、主动脉开放30 min(T1)、关胸后(T2)、主动脉开放6 h(T3)、12 h(T4)和24 h(T5)通过肺动脉导管观察相关左心功能指标,于T0、T1、T3~T5时测血浆N端脑钠素前体肽(NT-proBNP)浓度。结果与T0时比较,两组MAP在T1~T4、肺动脉阻塞压(PAOP)在T2~T5、全身血管阻力(SVR)在T1~T5时均降低(P0.05或P0.01),两组每搏指数(SI)、心脏指数(CI)和左心室每博做功指数(LVSWI)在T1~T5时均升高(P0.05或P0.01)。与C组比较,G组PAOP在T5时降低,混合静脉血氧饱和度(SvO2)在T2~T5时升高,SI在T4、T5时升高,CI和LVSWI在T3~T5时升高,NT-proBNP在T4、T5时降低。结论异氟醚预处理对心脏联合瓣膜置换术患者主动脉开放12~24 h左心功能可能有改善作用。     

阿片受体在异氟醚延迟预处理减轻兔心肌缺血再灌注损伤中的作用

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.     

瑞芬太尼静脉麻醉在腹腔镜胆囊切除术中的应用

【目的】观察不同剂量瑞芬太尼静脉麻醉用于腹腔镜胆囊切除术（LC）的临床效果.【方法】ASAⅠ～Ⅱ级择期行LC病人30例,年龄25～54岁,分为芬太尼（F）组,小剂量瑞芬太尼（L）组和大剂量瑞芬太尼（H）组,每组10例.记录术前,气管插管前、后等时点的血压、心率;记录术毕病人呼吸恢复、呼之睁眼、拔管和回病房时间;评估拔管后即刻、30 min、1 h、2 h伤口疼痛程度.【结果】①H组插管前后平均动脉压（MAP）和心率（HR）差异无显著性,且显著低于F、L组.②L、H组呼吸恢复、拔管、睁眼及回病房时间均早于F组.③L组于拔管后30 min、H组于拔管后1 h起VRS评分高于F组.【结论】瑞芬太尼麻醉应用于LC,有术后苏醒快的优点.瑞芬太尼0.75 μg/（kgmin）的速度持续输注在减少插管时的应激反应,维持术中到术后血流动力学平稳方面优于0.5 μg/（kgmin）的剂量.