氨溴索预先给药对兔单肺通气时肺损伤的影响

目的 评价氨溴索预先给药对兔单肺通气时肺损伤的影响.方法 家兔67只随机分为4组,麻醉下气管插管,机械通气,A组(n=18)持续双肺通气4 h,B组(n=16)、C组(n=15)和D组(n=18)单肺通气2 h后恢复双肺通气2 h,C组和D组在单肺通气前分别静脉注射氨溴索5、15 mg/kg(生理盐水稀释至20 ml),B组给予等容量生理盐水.分别于麻醉前(基础状态)、单肺通气1、2 h、恢复双肺通气1、2 h时采集静脉血样,测定血清超氧化物歧化酶(SOD)活性、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和IL-8浓度,进行白细胞(WBC)计数和中性粒细胞计数,最后一次采集血样后,处死动物,取双侧肺组织,光镜下观察肺组织病理学.结果 与A组比较,B组、C组和D组SOD活性降低,TNF-α、IL-6、IL-8、WBC计数和中性粒细胞计数升高(P<0.05或0.01).与B组比较,C组和D组SOD活性升高,TNF-α、IL-6、IL-8、WBC计数和中性粒细胞计数降低(P<0.05或0.01).C组和D组间上述指标差异无统计学意义(P>0.05).A组双侧肺组织未见明显损伤;C组和D组非通气侧肺组织损伤轻于B组.结论 静脉注射氨溴索5、15 mg/kg可减轻单肺通气诱发兔肺损伤,其机制与抑制炎性反应及脂质过氧化反应有关.     

电针足三里穴对兔肺缺血再灌注损伤的影响

目的探讨电针足三里穴对兔肺缺血再灌注损伤的影响及其机制。方法健康成年雄性新西兰家兔28只,体重1．7～2．3kg,随机分为4组,每组7只,假手术组（A组）：左侧开胸游离支气管和肺动脉、肺静脉后机械通气180min；缺血再灌注组（B组）：左侧开胸游离支气管和肺动脉、肺静脉后阻断左肺门60min后,开放左肺门行机械通气120min；非穴位＋缺血再灌注组（C组）：阻断左肺门60min后,开放左肺门行机械通气即刻电针双侧足三里穴旁5mm处30min,继续机械通气90min；足三里穴＋缺血再灌注组（D组）：阻断左肺门60min后,开放左肺门机械通气即刻电针双侧足三里穴30 min,继续机械通气90min。记录各组缺血30、60min、再灌注30、45、60、90、120min时平均动脉压（MAP）和心率（HR）,颈动脉抽血,行动脉血气分析,抽血后立即处死大鼠,取左肺,测定丙二醛（MDA）和髓过氧化物酶（MPO）水平及肺组织湿/干重比（W/D）。结果各组HR差异无统计学意义（P＞0．05）；与A组比较,C组再灌注90、120min MAP降低,B组和C组肺组织MDA和MPO水平、W/D及PaCO2升高,pH值和PaO2降低（P＜0．05或0．01）；与B组比较,C组再灌注期间MAP降低,D组肺组织MDA和MPO水平、W/D及PaCO2降低,pH值和PaO2升高（P＜0．05或0．01）。结论电针足三里穴可明显减轻家兔肺缺血再灌注损伤,其机制可能与降低脂质过氧化反应、抑制中性粒细胞的浸润有关。     

经皮穴位电刺激对单肺通气期间氧合和肺内分流的影响

目的：观察开胸手术中经皮电刺激穴位对单肺通气期间肺氧合及肺内分流的影响。方法：将择期开胸手术患者46例随机分为经皮穴位电刺激组（E组）和对照组（C组）。E组在麻醉诱导前30min开始经皮电刺激两侧孔最、肺俞穴。分别于平卧双肺通气30min（T1）、侧卧双肺通气30min（T2）、单肺通气15min（T3）、30min（T4）、60min（T5）各时点抽取桡动脉血及中心静脉导管血2mL,检测和计算pH、PaCO2、PaO2、SaO2、PvO2、SvO2、Hb、Qs/Qt。结果：两组患者PaO2、SaO2在单肺通气（T3、T4、T5）后开始下降（P〈0.05）,E组在T3、T4、T5时点明显高于C组（P〈0.05）。两组患者Qs/Qt在单肺通气（T3、T4、T5）后开始升高,E组在T3、T4、T5时点明显低于C组（P〈0.05）。结论：经皮电刺激孔最、肺俞穴位可以降低单肺通气时的肺内分流率,改善肺的氧合作用。     

Clara细胞分泌蛋白对兔单肺通气肺损伤的保护作用

目的 观察Clara细胞分泌蛋白(CCSP)对兔单肺通气肺损伤的保护作用.方法 30只新西兰大白兔随机均分为三组:双肺通气3 h组(Ⅰ组);单肺通气2 h,随后双肺通气1 h组(Ⅱ组);单肺通气Clara细胞剥除组(Ⅲ组)(通气方法同Ⅱ组).观察支气管Clara细胞百分率、血清和肺泡灌洗液(BALF)中CCSP含量、BALF中白细胞计数及中性粒细胞比值、血清肿瘤坏死因子α(TNF-α)、白细胞介素(IL)-6、IL-8水平、肺组织湿/干比值和肺组织病理学检查.结果 Clara细胞百分率、CCSP含量Ⅰ组高于Ⅱ组(P<0.05),Ⅱ组高于Ⅲ组(P(0.01);BALF中白细胞计数、中性粒细胞比值和血清中TNF-α、IL-6、IL-8水平、肺湿/干比值Ⅰ组低于Ⅱ组(P<0.05),Ⅱ组低于Ⅲ组(P<0.01);病理学检查示肺损伤程度Ⅰ组轻于Ⅱ组,Ⅱ组轻于Ⅲ组.结论 Clara细胞分泌蛋白可减轻单肺通气所致肺损伤.     

低潮气量单肺通气复合呼气末正压对开胸患者免疫功能的影响

目的观察低潮气量单肺通气复合呼气末正压对开胸术患者免疫功能的影响。方法选择ASAⅠ～Ⅱ级择期行开胸手术的病人30例,全麻后插入双腔支气管导管,侧卧位后,行双肺通气,待开胸后行单肺通气。所有病例按单肺通气模式不同分为3组：C组：传统单肺通气;P1组：低潮气量单肺通气复合呼气末正压通气;P2组：单肺通气时。每维均在相同时间点记录呼吸力学参数、血流动力学指标,并作血气分析,检测血浆IL-6、IL-8、IL-10的表达,观察T淋巴细胞亚群以及免疫球蛋白的变化。结果单肺通气时P1、P2两组与C组相比：气道峰压（Ppeak）明显下降（P〈0．01）,PaCO2升高（P〈0．05）,PaO2升高（P〈0．05）,MAP、HR无显著差异;血浆IL-6和IL-8释放减少,IL-10释放增多;与C组相比P1、P2两组免疫功能抑制减弱。结论低潮气量单肺通气复合呼气末正压通气可改善单肺通气氧合、降低气道压、减少炎症反应以及免疫抑制引起的肺损伤。     

电针对肢体缺血再灌注诱发兔肺损伤的影响

目的:观察电针肺俞穴和足三里穴对肢体缺血再灌注诱发兔肺损伤的影响。方法:40只健康雄性新西兰大白兔,采用随机数字表法分为假手术组、模型组、电针组和非穴位电针组(每组n=10)。采用夹闭股动脉3 h、再灌注4 h的方法制备兔肢体缺血再灌注损伤模型。电针组于模型制备前1～4 d(30 min/次,1次/d)及模型制备过程中电针肺俞穴和足三里穴(疏密波,刺激电流l～2 mA,频率2/15 Hz,波宽0.2～0.6 ms,以兔出现轻微肌颤为宜);非穴位电针组以相同的参数电针刺激肺俞穴和足三里穴旁开0.5 cm非经非穴处。再灌注4 h时处死兔,取肺组织行肺损伤评分,计算肺湿/干重(W/D)比值;测定肺组织髓过氧化物酶(MPO)活性、Western blotting法检测肺组织核因子-κBp65 (NF-κBp65)及细胞间黏附分子-1(ICAM-1)蛋白表达水平。结果:模型组、电针组和非穴位电针组再灌注4 h时肺组织W/D比值分别为6.75±0.36、4.90±0.23、6.68±0.39,均明显高于假手术组(3.09±0.15, P0.05);上述三组肺损伤评分分别为8.12±1.05、4.38±0.64、8.23±0.98,均明显高于假手术组(0.87±0.29, P0.05);上述三组MPO活性分别为(5.18±0.45)U/g、(3.76±0.33) U/g、(5.24±0.39) U/g,均明显高于假手术组[(1.59±0.25) U/g,P0.05];与假手术组相比,模型组、电针组和非穴位电针组ICAM-1及NF-κBp65表达水平升高;与模型组比较,电针组再灌注4 h时肺组织W/D比值、肺损伤评分、MPO活性、ICAM-1及NF-κBp65表达水平降低(P0.05)。结论:电针肺俞穴和足三里穴可减轻肢体缺血再灌注诱发的兔肺损伤,其机制可能与抑制NF-κB激活,从而减少ICAM-1介导的中性粒细胞聚集有关。     

外源性肺表面活性物质对呼吸机相关性肺损伤大鼠炎性反应的影响

目的 探讨外源性肺表面活性物质(PS)对呼吸机相关性肺损伤(VILI)大鼠炎性反应的影响.方法 成年雄性Wistar大鼠28只,体重310-388 g,采用随机数宁表法,将大鼠随机分为4组(n=7),对照组(C组)、VILI组、PS组和空气对照组(A组).采用高气道压机械通气(气道峰压40cmH2O,通气频率20次/min,PEEP 0)20 rin制备VILI模型.C组麻醉后即经股动脉放血处死.VILI 组于模型制备成功后放血处死.PS组和A组造模后采用自制吸痰管吸除气道内水肿液后经气道分别注入PS 100 mg/kg(50 mg/ml)和等容量空气,行机械通气(VT10 ml/kg,通气频率45次/min,PEEP 7.5cm H2O)120 min后放血处死.采集股动脉血样及气道内水肿掖,采用ELISA法测定血浆IL-6、IL-10、巨噬细胞炎性蛋白-2(MIP-2)和TNF-α浓度,采用Bradford蛋白浓度测定法测定气道内水肿液蛋白浓度.光镜下观察肺组织病理学及中性粒细胞数目.结果 4组血浆TNF-α浓度比较差异无统计学意义(P ＞0.05).与C组比较,VILI组血浆MIP-2、IL-10和IL-6浓度及中性粒细胞计数升高(P＜0.05),气道水肿液量和水肿液蛋白浓度比较差异无统计学意义(P＞0.05).与A组比较,PS组中性粒细胞计数减少(P＜0.05),气道水肿液量和水肿液蛋白浓度比较差异无统计学意义(P＞0.05),血浆MIP-2、IL-10和IL-6浓度差异无统计学意义(P＞0.05).VILI组、A组和PS组肺组织炎性损伤明显.结论 外源性PS治疗VILI大鼠可减少肺组织中性粒细胞募集,但不能抑制炎性细胞因子的释放.     

不同剂量瘦素对大鼠机械通气肺损伤的影响

目的评价不同剂量瘦素对大鼠机械通气肺损伤的影响。方法健康清洁级SD雄性大鼠48只,6～8周龄,采用随机数字表法分为四组:气管切开保留自主呼吸的假手术组(A组)、机械通气模型组(B组)、瘦素10μg/kg组(C组)和瘦素50μg/kg组(D组),每组12只。采用10%水合氯醛3.5 ml/kg麻醉大鼠,疼痛反射消失后C组腹腔注射瘦素10μg/kg,D组腹腔注射瘦素50μg/kg,A、B组腹腔注射等容量生理盐水,注射后即刻进行气管切开,插管机械通气。A组气管插管后保留自主呼吸,B、C、D组机械通气建立VILI模型,参数设置:V_T 20 ml/kg,RR 80次/分,I∶E 1∶1,FiO_2 21%,PEEP 0 mmHg,通气时间4 h。分别于基础状态、通气结束时抽取股动脉血进行血气分析。通气结束后放血处死大鼠,在4℃下取肺组织并收集支气管肺泡灌洗液(bronchoalveolar lavage fluid, BALF),光镜下进行中性粒细胞计数,采用ELISA法测定TNF-α、IL-6、IL-1β浓度;取肺组织称重,计算肺湿干重比(W/D);观察肺组织病理改变并进行病理评分;采用Western blot检测肺组织研磨液中NF-κB p65含量。结果与A组比较,B、C、D组W/D、肺损伤评分、BALF中性粒细胞计数、TNF-α、IL-6、IL-1β浓度及肺组织NF-κB p65含量明显升高(P0.01)。与B组比较,C、D组BALF中性粒细胞计数、TNF-α、IL-6、IL-1β浓度及肺组织肺损伤评分、NF-κB p65含量明显降低(P0.05)。与C组比较,D组BALF中性粒细胞计数、TNF-α、IL-6、IL-1β浓度及肺组织肺损伤评分、NF-κB p65含量明显降低(P0.05)。结论瘦素可降低大鼠机械通气肺损伤中炎性因子的表达水平,减轻肺损伤,50μg/kg较10μg/kg作用明显。     

亚甲蓝对兔肠缺血再灌注时肺损伤的影响

目的评价亚甲蓝（MB）对兔肠缺血再灌注时肺损伤的影响。方法健康新西兰白兔36只,体重2.5～3.5 kg,雄雌不拘,随机分为3组（n=12）,假手术组（S组）不夹闭肠系膜上动脉;缺血再灌注组（I/R组）：夹闭肠系膜上动脉1 h,再灌注3 h;MB组再灌注前即刻静脉注射亚甲蓝10 mg/kg。再灌注3 h时,抽取静脉血,测定血清肿瘤坏死因子-α（TNF-α）、白细胞介素-8（IL-8）及总蛋白浓度;取右肺下叶组织,测定肺组织湿/干重比（W/D）和Na^＋-K^＋-ATPase活性;测定支气管肺泡灌洗液（BALF）中蛋白浓度,并计算其与血清总蛋白浓度的比值,表示肺通透指数;光镜及电镜下观察肺组织结构,并进行中性粒细胞（PMN）计数。结果与S组比较,I/R组血清TNF-α、IL-8浓度及BALF蛋白浓度、PMN计数、肺通透指数和W/D升高,Na^＋-K^＋-ATPase活性降低,MB组PMN计数、BALF蛋白浓度和肺通透指数升高,Na^＋-K^＋-ATPase活性降低（P〈0.05或0.01）;与I/R组比较,MB组血清TNF-α、IL-8及BALF蛋白浓度、PMN计数、肺通透指数和W/D降低,Na^＋-K^＋-ATPase活性升高（P〈0.05或0.01）。MB组肺组织结构损伤轻于I/R组。结论再灌注前即刻静脉注射亚甲蓝10 mg/kg可减轻兔肠缺血再灌注时肺损伤,与抑制肺组织Na^＋-K^＋-ATPase活性降低及减轻炎性反应有关。     

肺动脉灌注抗肿瘤坏死因子-α抗体减轻体外循环的肺损伤

目的 探讨经肺动脉灌注抗肿瘤坏死因子-α抗体（TNF-αAb）对体外循环（CPB）肺损伤的保护作用及机制。 方法 健康新西兰大白兔40只,体重2.0～2.5 kg,雌雄不拘,随机分为4组,每组10只。Ⅰ组：CPB ＋单纯肺动脉灌注液;Ⅱ组：CPB ＋肺动脉灌注TNF-αAb;Ⅲ组：单纯CPB组;Ⅳ组：单纯开胸。测定4组CPB前、后左、右心房血液中性粒细胞计数、肿瘤坏死因子-α （TNF-α）、丙二醛（MDA）含量及氧合指数;取肺组织样本,在光学显微镜和电子显微镜下观察其病理变化和超微结构改变,并动态观察肺组织含水量、TNF-α mRNA表达及凋亡指数变化。 结果 与Ⅳ组比较,CPB后Ⅰ～Ⅲ组血浆中性粒细胞计数、TNF-α、MDA含量、肺组织TNF-α mRNA表达、凋亡指数均显著升高（P＜0.05）;肺组织含水量增加,而氧合指数显著下降（P＜0.05）,肺组织病理形态学发生改变。与Ⅱ组比较,CPB后Ⅰ组、Ⅲ组血浆TNF-α含量显著升高［主动脉开放5 min： （220.43±16.44） pg/ml vs. （185.27±11.78） pg/ml,P＜0.05; （249.99±14.09） pg/ml vs. （185.27±11.78） pg/ml,P＜0.05］,凋亡指数均显著升高（CPB停止即刻：60.7‰±13.09‰ vs. 37.9‰±7.78‰,P＜0.05;59.6‰±7.74‰ vs. 37.9‰±7.78‰,P＜0.05）,血浆中性粒细胞计数、MDA含量、肺组织TNF-α mRNA表达亦显著升高（P＜0.05）,肺组织含水量增加,而氧合指数显著下降（P＜0.05）,肺组织病理形态学改变明显。与Ⅰ组比较,Ⅲ组上述指标仅在CPB30 min显著升高（P＜0.05）,氧合指数显著下降（P＜0.05）。 结论 TNF-αAb经肺动脉灌注可明显抑制CPB期间炎性肺损伤,并减少肺组织细胞凋亡的发生。     

星状神经节阻滞对兔机械通气所致肺损伤的保护作用

目的 探讨星状神经节阻滞(stellate ganglion block,SGB)对兔呼吸机相关性肺损伤(ventilator associated lunginjury,VALI)的影响. 方法 40只成年日本大耳兔按随机数字表法分为两组(每组20只):空白对照组(Ⅰ组)和SGB组(Ⅱ组).Ⅰ组全身麻醉气管插管后椎旁注入生理盐水(0.5 ml),Ⅱ组全身麻醉气管插管后给予SGB.分别于机械通气后1 h(T1)、2 h(T2)、4 h(T3)、6 h(T4)4个时间点经耳缘静脉抽取静脉血3ml后处死白兔,检测血清丙二醛(malondialdehyde,MDA)、TNF-α浓度及超氧化物歧化酶(superoxide dismutase,SOD)活性;取左肺组织测量湿/干重比(wet/dry,W/D);取一部分右肺组织H-E染色后光镜和电镜观察其病理变化,另一部分匀浆后检测MDA含量、髓过氧化物酶(myeloperoxidase,MPO)及SOD活性. 结果 与Ⅰ组比较,Ⅱ组肺组织的W/D[(6.07±0.12)比(8.58±0.48)]和SOD活性[(64±10) U/mg比(77±11) U/mg]明显降低(P＜0.01);Ⅱ组肺组织的MDA含量[(0.89±0.12) μmol/g比(0.63±0.11) μmoFg]和MPO活性[(0.46±0.09) U/g比(0.28±0.07)U/g]明显升高(P＜0.01).H-E染色后光镜和电镜观察Ⅱ组肺组织病变轻于Ⅰ组.与Ⅰ组比较,Ⅱ组血清MDA、TNF-α在T2～T4时间点降低(P＜0.05),Ⅱ组血清SOD在T2-T4时间点升高(P＜0.05). 结论 SGB可以减轻机械通气兔肺组织的损伤,产生肺保护作用.     

Mechanical Ventilation Affects Lung Function and Cytokine Production in an Experimental Model of Endotoxemia

Background: Mechanical ventilation using tidal volumes around 10 ml/kg and zero positive end-expiratory pressure is still commonly used in anesthesia. This strategy has been shown to aggravate lung injury and inflammation in preinjured lungs but not in healthy lungs. In this study, the authors investigated whether this strategy would result in lung injury during transient endotoxemia in the lungs of healthy animals.

Methods: Volume-controlled ventilation with a tidal volume of 10 ml/kg and zero positive end-expiratory pressure was applied in two groups of anesthetized-paralyzed rabbits receiving either intravenous injection of 5 [mu]g/kg Escherichia coli lipopolysaccharide (n = 10) or saline (n = 10) 2 h after the start of mechanical ventilation. The third group consisted of 10 spontaneously breathing anesthetized animals receiving lipopolysaccharide. Anesthesia was then continued for 4 h in the three groups while the ventilatory modes were maintained unchanged. Lung injury was studied using blood gases, respiratory physiologic variables, analysis of the bronchoalveolar lavage cell counts, and cytokine concentrations and lung pathologic examination.

Results: Significant histologic lung alterations, hypoxemia, and altered lung mechanics were observed in rabbits treated with mechanical ventilation and intravenous lipopolysaccharide but not in the mechanically ventilated animals injected with saline or in spontaneously breathing animals treated with lipopolysaccharide. Endotoxemic ventilated animals also had significantly more lung inflammation as assessed by the alveolar concentration of neutrophils, and the concentrations of the chemokines interleukin 8 and growth-related oncogen [alpha].     

Treatment of Pulmonary Hypertension and Hypoxia Due to Oleic Acid Induced Lung Injury with Intratracheal Prostaglandin E1 during Partial Liquid Ventilation

Background: Partial liquid ventilation using perfluorocarbon liquids may be of therapeutic benefit in patients with acute respiratory failure. This study investigated the effects of prostaglandin E1 (PGE1) delivered intratracheally during partial liquid ventilation on lung function and pulmonary circulation in rabbits with acute respiratory distress syndrome.

Methods: Lung injury was induced by intravenous oleic acid in adult Japanese white rabbits, 1 h after which they were divided into four groups of 10 animals. Group 1 received mechanical ventilation alone, group 2 received aerosolized PGE1 (5 [micro sign]g followed by 0.1 [micro sign]g [middle dot] kg-1 [middle dot] min-1) under mechanical ventilation combined with 5 cm H2 O positive end-expiratory pressure, and groups 3 and 4 received partial liquid ventilation with 15 ml/kg perflubron. Group 4 received a 5-[micro sign]g bolus followed by 0.1 [micro sign]g [middle dot] kg-1 [middle dot] min-1 PGE1 instilled intratracheally (not by aerosol) in combination with partial liquid ventilation. Measurements were performed at 30-min intervals for 120 min after lung injury.

Results: After lung injury, hypoxemia, hypercapnia, acidosis, and pulmonary hypertension developed in all animals and were sustained in groups 1 and 2 throughout the experiment. The partial pressure of oxygen in arterial blood of animals in group 3 improved with initiation of treatment, with statistical significance achieved at the 30 and 60 min time points as compared with controls. Group 4 animals had immediate and sustained increases in the partial pressure of oxygen in arterial blood that were significant compared with all other groups during the experiment. Statistically significant reductions in mean pulmonary artery pressure were seen only in group 4 animals compared with all other groups.     

Nrf2 / HO-1通路在电针减轻肢体缺血再灌注诱发兔肺损伤中的作用

目的:观察核因子E2相关因子2(Nrf2)/血红素氧合酶-1(HO-1)信号通路在电针减轻肢体缺血再灌注诱发兔肺损伤中的作用。方法:40只健康雄性新西兰大白兔,采用随机数字表法分为假手术组、模型组、电针组和全反式维甲酸组(n=10)。采用夹闭股动脉3 h、再灌注4 h的方法制备兔肢体缺血再灌注模型;电针组、全反式维甲酸组于模型制备前1～4 d(30 min/次,1次/d)及模型制备过程中电针足三里穴和肺俞穴,采用疏密波2/15 Hz,强度以兔出现轻微肌颤为宜;全反式维甲酸组于模型制备前30 min腹腔注射Nrf2抑制剂全反式维甲酸7 mg/kg。再灌注4 h时采集颈动脉血样,随后处死兔取肺组织,观察病理学结果并行肺损伤评分,计算肺湿/干重(W/D)比值;测定肺组织MDA含量及SOD活性,采用Western blotting法检测肺组织Nrf2总蛋白、Nrf2核蛋白及HO-l蛋白表达水平。结果:模型组、电针组和全反式维甲酸组再灌注4 h时肺损伤评分分别为5.43±0.82、4.03±0.56、6.21±0.75,均明显高于假手术组(0.92±0.21,P0.05);肺组织W/D比值分别为6.42±1.00、4.45±0.68、7.08±1.12,均明显高于假手术组(2.04±0.29,P0.05);MDA含量分别为(4.82±0.51)nmol/mg、(3.56±0.45)nmol/mg、(5.18±0.47)nmol/mg,均明显高于假手术组(2.10±0.23)nmol/mg,P0.05;SOD活性分别为(50.6±6.3)U/mg、(63.1±7.7)U/mg、(47.2±5.6)U/mg,均明显低于假手术组(72.6±6.3)U/mg,P0.05;Nrf2总蛋白、Nrf2核蛋白及HO-l蛋白表达水平均明显高于假手术组(P0.05)。与模型组比较,电针组再灌注4 h时肺损伤评分、肺组织W/D比值、MDA含量均明显降低(P0.05),SOD活性、Nrf2总蛋白、核蛋白及HO-l蛋白表达水平均明显升高(P0.05)。与电针组比较,全反式维甲酸组再灌注4 h时肺损伤评分、肺组织W/D比值、MDA含量均明显升高(P0.05),SOD活性、Nrf2总蛋白、核蛋白及HO-l蛋白表达水平均明显降低(P0.05)。结论:Nrf2/HO-1信号通路激活参与了电针减轻肢体缺血再灌注诱发兔肺损伤的过程。     

Exogenous Surfactant Preserves Lung Function and Reduces Alveolar Evans Blue Dye Influx in a Rat Model of Ventilation-induced Lung Injury

Background: Changes in pulmonary edema infiltration and surfactant after intermittent positive pressure ventilation with high peak inspiratory lung volumes have been well described. To further elucidate the role of surfactant changes, the authors tested the effect of different doses of exogenous surfactant preceding high peak inspiratory lung volumes on lung function and lung permeability.

Methods: Five groups of Sprague-Dawley rats (n = 6 per group) were subjected to 20 min of high peak inspiratory lung volumes. Before high peak inspiratory lung volumes, four of these groups received intratracheal administration of saline or 50, 100, or 200 mg/kg body weight surfactant; one group received no intratracheal administration. Gas exchange was measured during mechanical ventilation. A sixth group served as nontreated, nonventilated controls. After death, all lungs were excised, and static pressure-volume curves and total lung volume at a transpulmonary pressure of 5 cm H2 O were recorded. The Gruenwald index and the steepest part of the compliance curve (Cmax) were calculated. A bronchoalveolar lavage was performed; surfactant small and large aggregate total phosphorus and minimal surface tension were measured. In a second experiment in five groups of rats (n = 6 per group), lung permeability for Evans blue dye was measured. Before 20 min of high peak inspiratory lung volumes, three groups received intratracheal administration of 100, 200, or 400 mg/kg body weight surfactant; one group received no intratracheal administration. A fifth group served as nontreated, nonventilated controls.

Results: Exogenous surfactant at a dose of 200 mg/kg preserved total lung volume at a pressure of 5 cm H2 O, maximum compliance, the Gruenwald Index, and oxygenation after 20 min of mechanical ventilation. The most active surfactant was recovered in the group that received 200 mg/kg surfactant, and this dose reduced minimal surface tension of bronchoalveolar lavage to control values. Alveolar influx of Evans blue dye was reduced in the groups that received 200 and 400 mg/kg exogenous surfactant.     

INCREASE IN TRACHEAL PRESSURE DURING JET VENTILATION

The effects of high frequency ventilation in combination withsustained inflations was studied in the surfactant-deficientlungs of 18 New Zealand White rabbits (weight 1.9–2.1kg) during anaesthesia with urethane and neuromuscu-lar blockwith pancuronium. Lung damage was induced by repeated lung lavage.In nine rabbits (group I) baseline ventilator settings weremaintained constant throughout the study and airway pressurewas readjusted to achieve a constant tidal volume. In the othernine rabbits (group II), ventilation was reinstituted afterlung lavage with one period of four sustained inflations followedimmediately by high frequency ventilation. In group I therewas a significant decrease in gas exchange for oxygen and deteriorationin pulmonary mechanics, whereas in group II there was littlechange in baseline blood-gas values or pulmonary mechanics.These data suggest that, with adequate ventilatory managementduring the period of lung lavage, the lung damage produced bythis manoeuvre may be obviated     

INFLUENCE OF HIGH FREQUENCY VENTILATION AT DIFFERENT END-EXPIRATORY LUNG VOLUMES ON THE DEVELOPMENT OF LUNG DAMAGE DURING LUNG LAVAGE IN RABBITS

The effects of high frequency ventilation in combination withsustained inflations was studied in the surfactant-deficientlungs of 18 New Zealand White rabbits (weight 1.9–2.1kg) during anaesthesia with urethane and neuromuscu-lar blockwith pancuronium. Lung damage was induced by repeated lung lavage.In nine rabbits (group I) baseline ventilator settings weremaintained constant throughout the study and airway pressurewas readjusted to achieve a constant tidal volume. In the othernine rabbits (group II), ventilation was reinstituted afterlung lavage with one period of four sustained inflations followedimmediately by high frequency ventilation. In group I therewas a significant decrease in gas exchange for oxygen and deteriorationin pulmonary mechanics, whereas in group II there was littlechange in baseline blood-gas values or pulmonary mechanics.These data suggest that, with adequate ventilatory managementduring the period of lung lavage, the lung damage produced bythis manoeuvre may be obviated.     

胸腔镜辅助下双侧肺静脉隔离治疗心房颤动的麻醉管理

目的 总结胸腔镜辅助下肺静脉隔离及左心耳切除术(Wolf Mini-maze手术)治疗心房颤动(房颤)的麻醉管理经验.方法 回顾性分析了14例接受Wolf Mini-maze手术患者的临床资料.术中对患者实施左、右肺单肺通气,射频消融前后进行电生理检查.分别记录左肺和右肺单肺通气开始前(T1),开始后15 min(T2...     

Peritoneal ventilation in rabbits: augmentation of gas exchange with cisapride.

BACKGROUND: Peritoneal ventilation has been shown to be effective in achieving extrapulmonary oxygenation and carbon dioxide elimination in an animal model of severe adult respiratory distress syndrome (ARDS). Cisapride is a "prokinetic" agent (increases gastric emptying), that may increase the splanchnic circulation and thus favourably affect gas exchange in peritoneal ventilation. METHODS: Using Doppler ultrasound the effect of cisapride on the portal venous circulation was examined in eight spontaneously breathing rabbits and the effect of cisapride on gas exchange in five rabbits spontaneously breathing room air was compared with that of a control group who did not receive cisapride. Its effect on gas exchange in five rabbits with ARDS being treated with mechanical lung and peritoneal ventilation was compared with that of a control group, and its effect on gas exchange in five rabbits with ARDS treated with conventional ventilation was also compared with that of a control group. RESULTS: Enteral administration of cisapride increased portal venous blood velocity, as measured ultrasonographically, by a mean of 188% one hour after receiving the drug. In rabbits with ARDS being treated with both peritoneal ventilation and mechanical ventilation to the lungs, those receiving cisapride had arterial oxygen tensions 1.5-3 times that of controls. Cisapride had no effect on arterial blood gas tensions in rabbits who were spontaneously breathing room air, nor in rabbits with ARDS who received only conventional mechanical lung ventilation. CONCLUSIONS: Cisapride increases arterial oxygenation in rabbits with severe ARDS treated with peritoneal ventilation, probably due to its ability to increase splanchnic circulation. It should be considered as an adjuvant medication to peritoneal ventilation.     

Changes in Pulmonary Blood Flow during Gaseous and Partial Liquid Ventilation in Experimental Acute Lung Injury

Background: It has been proposed that partial liquid ventilation (PLV) causes a compression of the pulmonary vasculature by the dense perfluorocarbons and a subsequent redistribution of pulmonary blood flow from dorsal to better-ventilated middle and ventral lung regions, thereby improving arterial oxygenation in situations of acute lung injury.

Methods: After induction of acute lung injury by repeated lung lavage with saline, 20 pigs were randomly assigned to partial liquid ventilation with two sequential doses of 15 ml/kg perfluorocarbon (PLV group, n = 10) or to continued gaseous ventilation (GV group, n = 10). Single-photon emission computed tomography was used to study regional pulmonary blood flow. Gas exchange, hemodynamics, and pulmonary blood flow were determined in both groups before and after the induction of acute lung injury and at corresponding time points 1 and 2 h after each instillation of perfluorocarbon in the PLV group.

Results: During partial liquid ventilation, there were no changes in pulmonary blood flow distribution when compared with values obtained after induction of acute lung injury in the PLV group or to the animals submitted to gaseous ventilation. Arterial oxygenation improved significantly in the PLV group after instillation of the second dose of perfluorocarbon.