盐酸戊乙奎醚预先给药对新生大鼠内毒素性急性肺损伤时NF-κB活性的影响

目的 探讨盐酸戊乙奎醚预先给药对新生大鼠内毒索性急性肺损伤时NF-kB活性的影响.方法 健康新生Wistar大鼠30只,雌雄不拘,日龄7 d,体重18～21 g,随机分为3组(n=10):对照组(C组)、急性肺损伤组(ALI组)和盐酸戊乙奎醚预先给药组(P组).采用腹腔注射内毒素3 mg/kg的方法制备急性肺损伤模型,P组腹腔注射盐酸戊乙奎醚0.5 mg/kg,30 min后制备模型,C组腹腔注射等容量生理盐水.于腹腔注射内毒素4 h时处死大鼠取肺,称重后计算肺湿,干重比,电镜下观察肺组织病理学结果,采用免疫组织化学法检测NF-kB p65的表达水平,采用酶联免疫吸附法测定TNF-α、IL-1 β及IL-10的含量.结果 与C组比较,ALI 组和P组肺湿/干重比、TNF-α、IL-1β、IL-10含量及NF-KB p65表达水平升高(P＜0.05);与ALI 组比较,P组肺湿/干重比、TNF-α、IL-1β、IL-10含量及NF-kBp65表达水平降低(P＜0.05).病理学结果显示:P组肺组织损伤程度较ALI组明显减轻.结论 盐酸戊乙奎醚预先给药可通过抑制肺组织NF-kB活化,降低炎性反应,减轻新生大鼠内毒素性急性肺损伤.     

盐酸戊乙奎醚在大鼠急性重症胰腺炎相关肺损伤中的作用

目的探讨盐酸戊乙奎醚在大鼠急性重症胰腺炎相关肺损伤(PALI)中的作用及对缺氧诱导因子(HIF)-1α相关炎症因子表达的影响。方法 40只健康雄性成年SD大鼠,应用随机数字法分为三组:假手术组(S组,n=8)、PALI模型组(ALI组,n=16)、盐酸戊乙奎醚+PALI模型组(P组,n=16)。ALI组和P组采用4%牛磺胆酸钠1ml/kg逆行性胰胆管注射法建立大鼠PALI模型。P组在建立模型后即刻给予大鼠腹腔内注射盐酸戊乙奎醚,S组和ALI组经腹腔注射等量生理盐水。造模后12h处死大鼠,取肺组织称重后计算肺湿干重比(W/D),光镜下观察胰腺及肺组织病理学评分,ELISA法测定肺组织HIF-1α、IL-1β、IL-6蛋白含量和血清胰淀粉酶含量,Western blot检测肺组织TLR4、NF-κB p65蛋白含量。结果 ALI组和P组大鼠的胰腺组织均存在广泛的中性粒细胞浸润、腺泡出血坏死和脂肪坏死。与S组比较,ALI组与P组胰腺病理评分、肺损伤评分、肺W/D明显升高,胰淀粉酶含量明显降低(P0.01);与ALI组比较,P组肺损伤评分、肺W/D明显降低(P0.05)。与S组比较,ALI组和P组大鼠肺组织HIF-1α、IL-1β、IL-6含量明显升高,肺组织TLR4、NF-κB p65含量明显升高(P0.01);与ALI组比较,P组肺组织HIF-1α、IL-1β、IL-6含量明显降低,TLR4、NF-κB p65蛋白含量明显降低(P0.05)。结论盐酸戊乙奎醚在不改变急性重症胰腺炎的胰腺组织损伤的情况下能够显著减轻急性重症胰腺炎相关肺损伤,机制可能与抑制HIF-1α等相关炎性因子的表达相关。     

盐酸戊乙奎醚预先给药对内毒素性急性肺损伤大鼠肺组织CD14和Toll样受体4表达的影响

目的 探讨盐酸戊乙奎醚预先给药对内毒素性急性肺损伤大鼠肺组织CD14和Toll样受体4(TLR4)表达的影响.方法 健康雄性SD大鼠32只,2月龄,体重230 ～ 280 g,采用随机数字表法,将大鼠随机分为4组(n=8),对照组(C组):腹腔和尾静脉均注射生理盐水1 ml/kg;急性肺损伤组(ALI组):腹腔注射生理盐水1 ml/kg,30 min后经尾静脉注射内毒素5 mg/kg;盐酸戊乙奎醚低剂量组(LP组)和高剂量组(HP组):分别腹腔注射盐酸戊乙奎醚0.3和1.0 mg/kg,30 min后经尾静脉注射内毒素5 mg/kg.静脉注射生理盐水或内毒素后6h时,取肺组织,分别采用Western blot法和RT-PCR法检测CD14、TLR4蛋白及其mRNA的表达水平,并观察肺组织病理学结果.结果 与C组比较,ALI组、LP组和HP组肺组织CD14、TLR4蛋白及其mRNA表达上调(P＜0.05);与ALI组比较,LP组及HP组肺组织CD14、TLR4蛋白及其mRNA表达下调(P＜0.05).LP组和HP组CD14、TLR4蛋白及其mRNA表达差异无统计学意义(P＞0.05).LP组和HP组肺组织病理学损伤较ALI组减轻.结论 盐酸戊乙奎醚预先给药可通过降低肺组织CD14、TLR4的活性减轻大鼠内毒素性急性肺损伤.     

盐酸戊乙奎醚预先给药对内毒素性急性肺损伤大鼠肺组织NF-κB mRNA表达及SOD活性的影响

目的 探讨盐酸戊乙奎醚预先给药对内毒素性急性肺损伤大鼠肺组织NF-κB mRNA表达及SOD活性的影响.方法 健康雄性SD大鼠32只,月龄2月,体重230～280 g,随机分为4组(n=8),对照组(C组)腹腔和尾静脉均注射生理盐水1 ml/kg;急性肺损伤组(ALI组):腹腔注射生理盐水1 ml/kg,30 min后经尾静脉注射LPS 5 mg/kg;盐酸戊乙奎醚低剂量组(LP组)、高剂量组(HP组)分别腹腔注射盐酸戊乙奎醚0.3和1 mg/kg,30 min后经尾静脉注射LPS 5 mg/kg.静脉注射生理盐水或LPS后6 h时,取肺组织,检测NF-κB mRNA的表达、TNF-α和MDA的含量和SOD活性,计算肺组织湿/干重比(W/D)及含水量,观察肺组织病理学结果.结果 与C组比较,ALI组、LP组和HP组肺组织NF-κB mRNA表达上调,TNF-α及MDA含量升高,SOD活性降低,W/D和肺组织含水量升高(P＜0.05);与ALI组比较,LP组和HP组肺组织NF-κB mRNA表达下调,TNF-α及MDA含量降低,SOD活性升高,W/D和肺组织含水量降低(P＜0.05);与LP组比较,HP组肺组织NF-κB mRNA表达下调,TNF-α及MDA含量降低,SOD活性升高,W/D和肺组织含水量降低(P＜0.05).LP组和HP组肺组织病理学损伤较ALI组减轻.结论 盐酸戊乙奎醚预先给药减轻大鼠内毒素性急性肺损伤的机制可能与下调肺组织NF-κB mRNA表达,降低肺局部炎性反应,增强机体抗氧化能力有关.     

盐酸戊乙奎醚预先给药对失血性休克大鼠急性肺损伤时NF-κB活性的影响

目的 探讨盐酸戊乙奎醚预先给药对失血性休克大鼠急性肺损伤时NF-κB活性的影响.方法 健康成年Wistar大鼠24只,体重200～250 g,雌雄不限,随机分为3组(n=8):假手术组(S组)、失血性休克致急性肺损伤组(ALI组)和盐酸戊乙奎醚预先给药组(P组).S组仅行动、静脉穿刺,不制备急性肺损伤模型;ALI组和P组经右侧颈内动脉穿刺置管监测BP,左侧股动脉置管放血,通过放血和回输血液维持BP 35～45 mm Hg 1 h,然后回输全部失血及等同于失血量的生理盐水,制备急性肺损伤模型;P组于放血前即刻静脉注射盐酸戊乙奎醚2 mg/kg. 于模型制备成功后6 h,采集右侧股动脉血样行血气分析,采用ELISA法测定右心房血浆TNF-α浓度,计算肺湿干重比,采用免疫组织化学法检测右肺组织NF-κB p65的表达,光镜下观察肺组织病理学.结果 与S组比较,Au组和P组PaO2降低,PaCO2、肺湿干重比、TNF-α浓度升高,NF-κB p65表达上调(P<0.05);与ALI组相比,P组PaO2升高,PaCO2、肺湿干重比、TNF-α浓度降低,NF-κB p65表达下调(P<0.05).病理结果显示:P组肺组织损伤较ALI组明显减轻.结论 盐酸戊乙奎醚预先给药可通过降低肺组织NF-κB的活性抑制炎性反应,从而减轻失血性休克诱发大鼠的急性肺损伤.     

盐酸戊乙奎醚预先给药对失血性休克大鼠急性肺损伤时TLR4 mRNA表达的影响

目的 探讨盐酸戊乙奎醚预先给药对失血性休克大鼠急性肺损伤时Toll样受体4(TLR4)mRNA表达的影响.方法 健康SD大鼠40只,体重200～250 g,随机分为5组(n=8):假手术组(S组)、失血性休克致急性肺损伤组(ALI组)和低、中、高剂量盐酸戊乙奎醚预先给药组(P1～3组).S组仅行动静脉穿刺,不放血,ALI组股动脉放血至35～45 mm Hg制备急性肺损伤模型,P1～3组分别于放血前30 min股静脉注射盐酸戊乙奎醚0.3、1.0、3.0 mg/kg,随后制备急性肺损伤模型.各组复苏后4 h时处死大鼠取肺,称重后计算肺湿干重比,检测TLR4 mRNA和NF-κB p65蛋白的表达水平,观察病理学结果.结果 与S组比较,ALI组和P1组TLR4 mRNA、NF-κB p65蛋白表达水平及肺湿干重比升高(P＜0.05或0.01),P2.3组差异无统计学意义(P＞0.05);与ALI组比较,P2,3组TLR4 mRNA、NF-κB p65蛋白表达水平及肺湿干重比降低(P＜0.05或0.01);P2组和P3组上述指标比较差异无统计学意义(P＞0.05).P2,3组肺组织病理学损伤程度较ALI组明显减轻.结论 盐酸戊乙奎醚预先给药可通过抑制肺组织TLR4 mRNA表达上调,进而降低NF-κB活性,从而减轻失血性休克诱发大鼠的急性肺损伤.     

戊乙奎醚预先给药对大鼠急性肺损伤时NF-κB的影响

目的 探讨戊乙奎醚预先给药对大鼠急性肺损伤(ALI)时NF-κB的影响.方法 雄性SD大鼠35只,体重210～280 g,随机分为5组(n=7):对照组(C组)、ALI组和低、中、高剂量戊乙奎醚组(P1-3组).采用经尾静脉注射内毒素5 mg/kg的方法建立大鼠ALI模型.C组和ALI组经腹腔注射生理盐水0.5 ml,P1～3组分别经腹腔注射戊乙奎醚0.03、0.1和3 mg/kg,30 min后ALI组、P1～3组制备AU模型,C组不制备模型.于静脉注射LPS后4 h时,行血气分析,计算氧合指数;称量肺组织湿重(W)、干重(D),计算W/D;采用比色法测定肺组织髓过氧化物酶(MPO)活性;采用RT-PCR法测定肺组织肿瘤坏死因子-α(TNF-α)mRNA、白细胞介素-1β(IL-1β)mRNA的表达水平;采用ELISA法测定肺组织TNF-α和IL-1β的含量;采用非放射性EMSA法测定肺组织NF-κB活性;采用免疫组织化学法测定肺组织NF-κB的表达水平.结果 与C组比较,其余各组氧合指数降低,肺组织W/D和MPO活性、TNF-α,IL-1β含量及其相应mRNA表达水平、NF-κB活性和表达水平均升高(P<0.05或0.01);与ALI组比较,P1～3组氧合指数升高,肺组织W/D和MPO活性降低,TNF-α、IL-1β含量及其相应mRNA表达水平降低,NF-κB活性和表达水平降低(P<0.05);P1～3组上述指标比较差异无统计学意义(P>0.05).结论 戊乙奎醚预先给药减轻大鼠急性肺损伤的机制可能与抑制NF-κB的活化,下调NF-κB的表达,降低肺组织炎性反应有关.     

盐酸戊乙奎醚对体外循环致大鼠急性肺损伤的影响

目的 评价盐酸戊乙奎醚对体外循环(CPB)致大鼠急性肺损伤的影响.方法 成年雄性SD大鼠40只,4～6月龄,体重330～420 g,采用随机数字表法,将其随机分为4组(n=10):假手术组(S组)仅进行动脉和静脉穿刺置管;急性肺损伤组(ALI组)、低剂量盐酸戊乙奎醚组(PL组)和高剂量盐酸戊乙奎醚组(PH组)建立CPB模型;PL组和PH组分别在预冲液中加入盐酸戊乙奎醚0.6和2.0 mg/kg,ALI组加入等容量生理盐水,进行CPB1h.于CPB前和CPB结束后2h采集动脉血样,进行血气分析;于CPB结束后2h时采集上腔静脉血样,测定血浆TNF-α和IL-6的浓度;取肺组织测定含水量、MDA含量和谷胱甘肽过氧化物酶(GSH-px)活性,光镜下观察病理学改变.结果 与S组比较,ALI组、PL组和PH组CPB结束后2h时PaO2降低,肺组织含水量、MDA含量和血浆TNF-α和IL-6的浓度升高,肺组织GSH-px活性降低(P＜0.05);与ALI组比较,PL组和PH组CPB结束后2h时PaO2升高,肺组织含水量、MDA含量和血浆TNF-α和IL-6的浓度降低,肺组织GSH-px活性升高(P＜0.05),病理学损伤减轻;与PL组比较,PH组CPB结束后2h时PaO2升高,肺组织含水量、MDA含量和血浆TNF-α和IL-6的浓度降低,肺组织GSH-px活性升高(P＜0.05),病理学损伤减轻更明显.结论 盐酸戊乙奎醚0.6和2.0 mg/kg可减轻CPB致大鼠急性肺损伤,且与剂量有关,其机制与抑制脂质过氧化反应和炎性反应有关.     

盐酸戊乙奎醚对新生大鼠内毒素性急性肺损伤时肺氧化应激和细胞凋亡的影响

目的评价盐酸戊乙奎醚对新生大鼠内毒素性急性肺损伤(acute lung injury,ALI)时肺氧化应激和细胞凋亡的影响。方法清洁级健康雄性Wistar大鼠30只,7日龄,体重12~18g。采用随机数字表法分为三组:盐酸戊乙奎醚组(PHC组)、ALI组和生理盐水组(NS组),每组10只。PHC组和ALI组大鼠腹腔注射内毒素5.0mg/kg制备ALI模型。PHC组于内毒素注射前1h腹腔注射盐酸戊乙奎醚2.0mg/kg,NS组和ALI组给予等容量生理盐水。于注射内毒素4h后处死大鼠取肺组织标本,计算肺湿/干重比(W/D),采用硫代巴比妥酸法测定丙二醛(MDA)浓度,黄嘌呤氧化酶法测定大鼠超氧化物歧化酶(SOD)活性,免疫组织化学法测定细胞色素C(Cyt-C)、半胱氨酸天冬蛋白酶-3(Caspase-3)的含量,TUNEL法计数凋亡细胞,计算细胞凋亡指数(AI)。结果与NS组比较,ALI组和PHC组肺W/D和MDA浓度明显升高,SOD活性明显降低(P0.05);与ALI组比较,PHC组肺W/D和MDA浓度明显降低,SOD活性明显升高(P0.05)。与NS组比较,ALI组和PHC组Cyt-C、Caspase-3含量和AI明显升高;与ALI组比较,PHC组Cyt-C、Caspase-3含量和AI明显降低(P0.05)。结论盐酸戊乙奎醚可能通过抑制肺组织氧化应激和细胞凋亡,减轻新生大鼠内毒素性急性肺损伤。     

盐酸戊乙奎醚预先给药对脓毒症小鼠急性肺损伤时肺组织β-arrestin-2表达的影响

目的 探讨盐酸戊乙奎醚预先给药对脓毒症小鼠急性肺损伤时肺组织p抑制蛋白-2(β-arrestin-2)表达的影响.方法 健康雌性昆明小鼠30只,6周龄,体重18～20 g,采用随机数字表法,将其随机分为3组(n=10):假手术组(S组)、脓毒症组(CLP组)和盐酸戊乙奎醚预先给药组(PHC组).CLP组和PHC组采用盲肠结扎并穿孔法制备脓毒症模型.PHC组于模型制备前1h时腹腔注射盐酸戊乙奎醚0.45 mg/kg,S组和CLP组于模型制备前1h时腹腔注射等容量生理盐水.模型制备后12h时,采血和收集肺泡灌洗液测定肺通透性指数,采用化学比色法测定肺组织MPO活性,采用ELISA法测定肺组织IL-6含量,采用Western blot法测定肺组织β-arrestin-2蛋白表达,采用RT-PCR法测定肺组织β-arrestin-2 mRNA表达.结果 与S组比较,CLP组肺通透性指数、肺组织MPO活性和IL-6含量均升高,肺组织β-arrestin-2蛋白表达下调,β-arrestin-2 mRNA表达上调(p＜0.05),PHC组肺通透性指数、肺组织MPO活性和IL-6含量均升高,肺组织β-arrestin-2蛋白表达上调,β-arrestin-2 mRNA表达下调(p＜0.05).与CLP组比较,PHC组肺通透性指数、肺组织MPO活件和IL-6含量均降低,肺组织β-arrestin-2蛋白表达上调,β-arrestin-2 mRNA表达下调(P＜0.05).结论 盐酸戊乙奎醚预先给药减轻脓毒症小鼠急性肺损伤的机制可能与上调肺组织β-arrestin-2的蛋白表达有关.     

Alveolar recruitment in acute lung injury

Alveolar recruitment is one of the primary goals of respiratorycare for acute lung injury. It is aimed at improving pulmonarygas exchange and, even more important, at protecting the lungsfrom ventilator-induced trauma. This review addresses the conceptof alveolar recruitment for lung protection in acute lung injury.It provides reasons for why atelectasis and atelectrauma shouldbe avoided; it analyses current and future approaches on howto achieve and preserve alveolar recruitment; and it discussesthe possibilities of detecting alveolar recruitment and derecruitment.The latter is of particular clinical relevance because interventionsaimed at lung recruitment are often undertaken without simultaneousverification of their effectiveness.     

单肺通气诱发肺损伤时兔肺组织线粒体转录因子A表达的变化

目的 探讨单肺通气诱发肺损伤时兔肺组织线粒体转录因子A(mtTFA)表达的变化.方法 健康雄性新西兰大白兔16只,体重2.5～3.0 kg,采用随机数字表法,将其分为2组(n=8)∶双肺通气组(TLV组)和单肺通气组(OLV组).气管切开插入自制双腔气管插管.TLV组双肺通气3h,OLV组左肺通气2h后再双肺通气1h.于通气开始即刻、通气1、2h、通气结束即刻采集动脉血样行血气分析,计算氧合指数.通气结束后开胸取左侧肺尖部组织,HE染色,光镜下观察病理学结果,行肺损伤评分,Western blot法检测肺组织mtTFA表达.结果 与TLV组比较,OLV组氧合指数降低,肺损伤评分升高,肺组织mtTFA表达下调(P＜0.05);OLV组肺组织病理学损伤程度严重.结论 单肺通气可能通过下调肺组织mtTFA表达诱发兔肺损伤.     

Transimission of donor lymphocytes in clinical lung transplantation

Passenger mononuclear cells in organ grafts are known to influence the alloimmune response to the graft. To assess their relevance in clinical lung transplantation, we studied the amount, distribution, cell types, and surface marker expression of mononuclear cells in human donor lungs. Two major compartments of mononuclear cells could be differentiated: lymph nodes containing resting T and B lymphocytes, and the lung tissue itself, containing mainly activated lymphocytes as well as monocytes/macrophages. Tissue-associated mononuclear cells make up 20–40x10⁹ cells per lung, about 30–50 % of which are lymphocytes. Tissue-associated lymphocytes are predominantly T and NK cells; most of the T cells are CD8⁺ CD45R0⁺ and express HLA-DR. Strong expression of the adhesion molecules LFA-1 and ICAM-1 is present on infiltrating cells as well as on resident cells of the organ. Moreover, the lymphocytes inside the lung tissue are functionally highly active, with a strong stimulatory as well as alloreactive potency. Thus, large numbers of allogeneic mononuclear cells and particularly large numbers of functionally active lymphocytes are obviously transmitted by human lung allografts. The immunological in vivo relevance of these cells after lung transplantation may include allostimulation and graft-versus-host activity, but also beneficial immunomodulatory effects.     

肺组织γ-氨基丁酸A型受体在大鼠内毒素诱发急性肺损伤中的作用

目的 探讨肺组织γ-氨基丁酸A型受体(GABAAR)在大鼠内毒素诱发急性肺损伤中的作用.方法 成年健康雄性Wistar大鼠32只,8周龄,体重200 ～ 230 g,采用随机数字表法,将其随机分为4组(n=8)∶正常对照组(C组)、内毒素组(LPS组)、γ-氨基丁酸预先给药+内毒素组(GABA组)和GABAAR拮抗剂荷包牡丹碱预先给药+内毒素组(BIC组).LPS组、GABA组和BIC组尾静脉注射LPS 5 mg/kg,C组给予等容量生理盐水;GABA组和BIC组分别于给予LPS前30 min时腹腔注射γ-氨基丁酸50 mg/kg和荷包牡丹碱10 μmol/kg.于给予LPS后6h时,采集动脉血样,测定PaO2,然后取肺组织,测定肺湿/干重比(W/D)、GABAAR表达、IL-6、TNF-α、MDA的含量和SOD活性,光镜下观察肺组织病理学结果.结果 与C组比较,LPS组、GABA组和BIC组PaO2降低,LPS组和GABA组肺组织W/D、TNF-α、IL-6和MDA的含量升高,肺组织GABAAR表达上调,肺组织SOD活性降低(P＜0.05);与LPS组比较,GABA组肺组织W/D、TNF-α、IL-6和MDA的含量升高,肺组织GABAAR表达上调,肺组织SOD活性降低(P＜0.05),而BIC组上述指标差异无统计学意义,GABA组和BIC组PaO2差异无统计学意义(P＞0.05).结论 肺组织GABAAR参与了大鼠内毒素诱发急性肺损伤的发展.     

Small dose of exogenous surfactant combined with partial liquid ventilation in experimental acute lung injury: effects on gas exchange, haemodynamics, lung mechanics, and lung pathology

A combination of exogenous surfactant and partial liquid ventilation(PLV) with perfluorocarbons should enhance gas exchange, improverespiratory mechanics and reduce tissue damage of the lung inacute lung injury (ALI). We used a small dose of exogenous surfactantwith and without PLV in an experimental model of ALI and studiedthe effects on gas exchange, haemodynamics, lung mechanics,and lung pathology. ALI was induced by repeated lavages (Pa_O2/FI_O2less than 13 kPa) in 24 anaesthesized, tracheotomized and mechanicallyventilated (FI_O2 1.0) juvenile pigs. They were treated randomlywith either a single intratracheal dose of surfactant (50 mgkg^–1, Curosurf^®, Serono AG, München, Germany)(SURF-group, n=8), a single intratracheal dose of surfactant(50 mg kg^–1, Curosurf^®) followed by PLV with 30 mlkg^–1 of perfluorocarbon (PF 5080, 3M, Germany) (SURF-PLV-group,n=8) or no further intervention (controls, n=8). Pulmonary gasexchange, respiratory mechanics, and haemodynamics were measuredhourly for a 6 h period. In the SURF-group, the intrapulmonaryright-to-left shunt (Q^·S/Q^·T) decreased significantlyfrom mean 51 (SEM 5)% after lavage to 12 (2)%, and Pa_O2 increasedsignificantly from 8.1 (0.7) to 61.2 (4.7) kPa compared withcontrols and compared with the SURF-PLV-group (P<0.05). Inthe SURF-PLV-group, Q^·S/Q^·T decreased significantlyfrom 54 (3)% after induction of ALI to 26 (3)% and Pa_O2 increasedsignificantly from 7.2 (0.5) to 30.8 (5.0) kPa compared withcontrols (P<0.05). Static compliance of the respiratory system(C_RS), significantly improved in the SURF-PLV-group comparedwith controls (P<0.05). Upon histological examination, theSURF-group revealed the lowest total injury score compared withcontrols and the SURF-PLV-group (P<0.05). We conclude thatin this experimental model of ALI, treatment with a small doseof exogenous surfactant improves pulmonary gas exchange andreduces the lung injury more effectively than the combined treatmentof a small dose of exogenous surfactant and PLV. Br J Anaesth 2001; 87: 593–601     

Fentanyl decreases end-expiratory lung volume in patients anaesthetized with sevoflurane

BACKGROUND: In patients breathing spontaneously during anaesthesia, expiratory muscle activity can be a prominent feature. This activity is triggered or exaggerated by opioid administration, which causes a prompt increase in intra-abdominal pressure. The effect of this increased expiratory activity on end-expiratory lung volume is not described. METHODS: Nine patients having minor gynaecological procedures were studied during stable anaesthetic conditions, breathing sevoflurane (end tidal 2.6%) through a laryngeal mask airway, in a circle system. The spill valve was closed and the fresh gas flow was temporarily reduced to approximate the oxygen uptake. The volume of the reservoir bag was then measured by placing it in a hinged, wedge-shaped container. Fentanyl (0.5 microg kg(-1) ideal body weight) was given after 1 min of stable recording, and the change in end-expiratory volume measured after 3 min. RESULTS: End-expiratory lung volume decreased in all patients by 160 (111) ml (mean, SD) (P<0.01). The decrease did not relate to obesity. CONCLUSIONS: During sevoflurane anaesthesia, fentanyl causes a rapid reduction in functional residual capacity. This is caused by increased activity of expiratory muscles and an increase in intra-abdominal pressure.     

Lobectomy for cavitating lung abscess with haemoptysis: strategy for protecting the contralateral lung and also the non-involved lobe of the ipsilateral lung

We describe the anaesthetic management of a patient undergoinglobectomy for cavitating lung abscess complicated by haemoptysis.Surgery for lung abscess is one of the absolute indicationsfor the use of a double-lumen tube (DLT). Because pus or bloodcould impede fibreoptic- assisted DLT placement, a traditional,blind placement of the DLT was performed. To protect the uninvolvedparts of the operated lung, ventilation of the lung with theabscess was not performed until the resection of the involvedlobe had been completed. Br J Anaesth 2000; 85: 791–4 ^* Corresponding author     

微量肺源性内毒素对大鼠呼吸机相关性肺损伤的影响

目的 评价微量肺源性内毒素对大鼠呼吸机相关性肺损伤的影响.方法 成年雄性SD大鼠32只,体重370～390 g,随机分为4组(n=8):自主呼吸组(C组)、内毒素+自主呼吸组(LC组)、机械通气组(M组)和内毒素+机械通气组(LM组).LC组和LM组气管内滴入内毒素100 μg/kg;M组和LM组行机械通气,潮气量20 ml/kg,呼气末正压0,1:E 1:1,维持P_(ET)CO_235～45 mm Hg;C组和LC组保持自主呼吸.于机械通气前、机械通气1、2和3 h时行血气分析,并记录血液动力学指标.机械通气3 h时放血处死大鼠,测定肺组织病理学损伤评分、湿/干重比(W/D比)、支气管肺泡灌洗液(BALF)中白细胞计数和肺蛋白透性系数,采用ELISA法检测血浆TNF-α和巨噬细胞炎性蛋白-2(MIP-2)的浓度.C组和M组采用RT-PCR法测定肺组织CD14 mRNA的表达水平,免疫组化法测定BALF中CD14的表达水平.结果 C组和M组血浆中未检测到TNF-α;与C组比较,LC组肺组织病理学损伤评分、W/D比、BALF中自细胞计数、肺蛋白透性系数和血浆MIP-2浓度差异无统计学意义(P>0.05),血浆TNF-α浓度升高,M组肺组织病理学损伤评分、BALF中白细胞计数和血浆MIP-2浓度升高,LM组肺组织病理学损伤评分、W/D比和BALF中白细胞计数、肺蛋白透性系数、血浆MIP-2和TNF-α的浓度升高(P<0.05或0.01);与M组比较,LM组肺组织病理学损伤评分、W/D比、BALF中自细胞计数、肺蛋白透性系数、血浆MIP-2和TNF-α的浓度升高(P<0.05或0.01).与C组比较,M组BALF中CD14表达和肺组织CD14 mRNA表达上调(P相似文献