七氟醚预处理对大鼠肺缺血再灌注时肺组织血管紧张素转化酶mRNA表达的影响

目的 探讨七氟醚预处理对大鼠肺缺血再灌注时肺组织血管紧张素转化酶(ACE) mRNA表达的影响.方法 成年雄性SD大鼠54只,体重250 ～ 320 g,采用随机数字表法,将其分为3组(n=18):假手术组(S组)仅游离左肺门,但不阻断;肺缺血再灌注组(I/R组)采用阻断左肺门45 min后再灌注120 min的方法制备大鼠肺缺血再灌注模型;七氟醚预处理组(SP组)吸入2.1％七氟醚30min,停止吸入后10 min时后制备肺缺血再灌注模型.于再灌注30、60和120 min时随机取6只大鼠,处死取肺组织,测定湿/干重比(W/D比),采用比色法测定髓过氧化物酶(MPO)活性,采用RT-PCR法测定ACE mRNA的表达,光镜下观察肺组织病理学结果.结果 与S组比较,I/R组和SP组再灌注各时点肺组织W/D比、MPO活性和ACE mRNA表达水平均升高(P＜0.05);与I/R组比较,SP组再灌注各时点肺组织W/D比、MPO活性和ACE mRNA表达水平降低(P＜0.05).SP组肺组织病理学损伤较I/R组减轻.结论 七氟醚预处理可能通过下调ACE mRNA的表达从而减轻大鼠肺缺血再灌注损伤.     

七氟醚对在体大鼠肺缺血-再灌注损伤的影响

目的研究七氟醚对在体大鼠肺缺血-再灌注(I-R)损伤的影响。方法40只Wistar大鼠建立在体大鼠肺I-R模型,随机分为四组,每组10只:A组,假手术组,开胸后机械通气120 min;B组,I-R组,阻断左肺门60 min,开放再通气60 min;C组,七氟醚加I-R组,缺血前吸入1 MAC七氟醚30 min,开放再通气同时吸入1 MAC七氟醚60 min;D组,七氟醚组,持续吸入1 MAC七氟醚120min。观察各组实验结束时肺组织的湿/干重比(W/D)、肺丙二醛(MDA)、超氧化物歧化酶(SOD)和肺组织病理学的改变。结果B组及C组肺W/D较A组和D组显著升高(P<0.01,P<0.05),SOD含量显著低于A组和D组(P<0.05);B组肺MDA含量较A组和D组显著升高(P<0.01),C组肺MDA含量较B组低(P<0.05);C组肺W/D、肺MDA显著低于B组(P<0.05),SOD高于B组(P<0.05);病理切片见B组、C组部分肺泡结构破坏,肺泡间隔增宽,肺泡腔内水肿并有出血,以B组改变较为严重,炎症积分显著高于C组(P<0.01)。结论七氟醚对在体大鼠肺I-R损伤有一定的保护作用。     

肺保护性通气策略对食管癌根治术老年患者单肺通气期间脑氧饱和度的影响

目的 评价肺保护性通气策略对食管癌根治术老年患者单肺通气期间脑氧饱和度(rSO2)的影响.方法 择期行食管癌根治术的患者40例,年龄65～76岁,体重45～75 kg,ASA分级Ⅰ～Ⅲ级,采用随机数字表法,将其随机分为2组(n=20):常规通气组(CV组)和保护性通气组(PV组).静脉注射咪达唑仑0.05 mg/kg、舒芬太尼0.4μg/kg、罗库溴铵1mg/kg和异丙酚1.5mg/kg麻醉诱导,左侧插入左侧双腔支气管导管进行机械通气.CV组双肺通气和单肺通气期间VT均为10 ml/kg,吸呼比均为1:2;PV组双肺通气和单肺通气期间VT均为6 ml/kg,吸呼比均为1:2,并给予PEEP 5cm H2O;两组维持PETCO235-45 mm Hgo吸入2％七氟醚,间断静脉注射罗库溴铵0.5 mg/kg维持麻醉.于麻醉诱导前、双肺通气10 min和单肺通气30 min时,进行动脉血气分析,计算肺内分流率(Qs/Qt),记录rSO7.记录单肺通气期间低rS02(rS02积分＞3000％)的发生情况.结果 与CV组比较,PV组单肺通气30 min时PaO2和rSO2升高,Qs/Qt降低,低rS)2发生率降低(P＜0.05).结论 肺保护性通气策略可改善食管癌根治术老年患者单肺通气期间的氧合,降低肺内分流,减少低rSO2,的发生.     

七氟醚预处理对大鼠内毒素性急性肺损伤的影响

目的 探讨七氟醚预处理对大鼠内毒素性急性肺损伤的影响.方法 健康雄性SD大鼠24只,体重220～250 g,随机分为4组(n=6):对照组(c组)、内毒素组(LPS组)、七氟醚组(Sev组)和七氟醚预处理组(SP组).C组和LPS组机械通气30 min后分别静脉注射生理盐水和脂多糖(LPS)5 mg/kg;Sev组和SP组吸入七氟醚(呼气末浓度2.4%)30 min,洗脱5 min,然后分别静脉注射生理盐水和LPS 5 mg/kg.于给予LPS或生理盐水后6 h时,心脏放血处死大鼠,取肺组织,计算湿重/干重(W/D)比;采用弥漫性肺泡损伤(DAD)评分评价肺组织损伤程度;测定肺组织髓过氧化物酶(MPO)活性、细胞因子诱导中性粒细胞化学趋化因子-1(CINC-1)含量、CINC-1和CINC-1 mRNA的表达水平.结果 与C组比较,LPS组和SP组肺组织W/D比、DAD评分、MPO活性和CINC-1含量升高,CINC-1和CINC-1 mRNA的表达上调(P<0.01),Sev组上述指标差异无统计学意义(P>0.05);与LPS组比较,SP组肺组织W/D比、DAD评分、MPO活性和CINC-1含量降低,CINC-1和CINC-1 mRNA的表达下调(P<0.01).结论 七氟醚预处理可减轻大鼠内毒素性急性肺损伤,可能与其抑制肺组织炎性反应有关.     

单肺通气期间七氟醚或丙泊酚对脑氧代谢的影响

目的观察单肺通气期间七氟醚或丙泊酚联合靶控持续输注瑞芬太尼对脑氧代谢的影响。方法选择行肺叶切除术患者30例,随机分为七氟醚组（S组）或丙泊酚组（P组）,每组各15例。麻醉诱导后,分别持续吸入七氟醚1%-2.5%或静脉持续泵入丙泊酚4-8 mg/（kg.h）。于双肺通气15 min（T1）,单肺通气15 min（T2）,单肺通气30 min（T3）,恢复双肺通气之后15min（T4）时点记录HR、MAP及BIS值,同时采集桡动脉、颈内静脉球血行血气分析,测定颈静脉球氧饱和度（SjvO2）,并计算脑动静氧含量差（AjvDO2）及COER值。结果两组在T2、T3时点的PaO2值较T1时点明显降低（P〈0.05）;S组各时点的SjvO2值、AjvDO2值、COER值与P组相应时点比较,无统计学差异（P〉0.05）。结论单肺通气过程中七氟醚与丙泊酚联合瑞芬太尼均能够达到满意麻醉效果,并保持脑氧供需平衡。     

L-精氨酸对兔肺缺血再灌注时血红素氧合酶-1的影响

目的 探讨L-精氨酸对兔肺缺血再灌注时血红素氧合酶-1(HO-1)的影响.方法 健康日本大耳白兔20只,雌雄不拘,体重1.7～2.6 kg,随机分为2组,肺缺血再灌注组(IR组)和L-精氨酸治疗组(L-Arg组),每组10只.建立兔单肺原位缺血再灌注损伤模型,L-Arg组肺缺血前20 min耳缘静脉注射L-Arg溶液100 mg/kg.采用原位杂交方法测定兔肺组织HO-1的表达;计算肺组织湿/干重比(W/D)及损伤肺泡百分数(IAR);电镜下观察肺组织超微结构.结果 HO-1在两组肺血管内皮、部分血管平滑肌、外膜层及部分气道上皮均有表达;与IR组比较,L-Arg组HO-1水平升高,W/D及IAR降低(P＜0.05);L-Arg组肺组织形态学异常改变轻于IR组.结论 L-精氨酸可通过上调肺组织HO-1的表达,增强肺组织HO-1的活性,减轻兔肺缺血再灌注损伤.     

肺癌根治术单肺通气前间断通气对非通气侧肺组织HIF-1α及靶基因HO-1的影响

目的探讨单肺通气(OLV)前间断通气对非通气侧肺组织缺氧诱导因子1α(HIF-1α)及靶基因血红素加氧酶-1(HO-1)的影响。方法选择择期全麻下行肺癌根治术的老年患者40例,男19例,女21例,年龄65~80岁,BMI 18~25kg/m2,ASAⅡ或Ⅲ级。采用随机数字表法,将患者均分为两组:对照组(C组)和间断通气预处理组(Y组)。两组麻醉诱导后行气管插管,机械通气。两组气管插管成功后立即改为OLV,C组非通气侧肺不做任何处理;Y组非通气侧肺用负压吸引器(压力0.06 MPa)吸引10s后开放于空气,5min后改为双肺通气,5min后再次改为OLV,重复上述操作,如此3个循环后改为双肺通气。于手术进胸后OLV即刻(T1)、OLV 60min(T2)和病变组织切除即刻(T3)分别切取肿瘤周边约2cm需手术一并切除的肺组织,一份经液氮保存,Western blot法检测HIF-1α及HO-1表达;余下肺组织置于多聚甲醛溶液中待检,光镜下观察肺组织损伤程度,并进行肺损伤评分。结果与T1时比较,T2、T3时两组PaO2明显降低(P0.05),T2时Y组HIF-1α表达明显升高,T3时两组HIF-1α和HO-1表达明显升高(P0.05);与T2时比较,T3时两组HIF-1α表达明显升高,Y组HO-1表达明显升高(P0.05);T2、T3时Y组HIF-1α表达明显高于C组,T3时Y组HO-1表达明显高于C组(P0.05)。与T1时比较,T3时两组肺损伤评分明显升高(P0.05);T3时Y组肺损伤评分明显低于C组(P0.05)。结论单肺通气前间断通气可减轻非通气侧肺塌陷期间肺损伤程度,其机制可能与增强塌陷侧肺组织HIF-1α及其靶基因HO-1表达有关。     

幼猪机械通气中异氟醚或七氟醚混合一氧化氮吸入的安全性

目的研究吸入异氟醚或七氟醚混合一氧化氮(NO)在幼猪机械通气中的安全性。方法36头幼猪随机分为6组:Ⅰ组(对照组):单纯机械通气;Ⅱ组(NO组):吸入20ppmNO;Ⅲ组(异氟醚组):吸入1.3MAC异氟醚;Ⅳ组(异氟醚 NO组):吸入1.3MAC异氟醚及20ppmNO;Ⅴ组(七氟醚组)吸入1.3MAC七氟醚;Ⅵ组(七氟醚 NO组)吸入1.3MAC七氟醚及20ppmNO。用麻醉机行间歇正压通气4h,测定各组机械通气前、机械通气1、2、3、4h(T0、T1、T2、T3、T4)的呼吸频率(RR)、呼吸系统总顺应性(Crs)、气道压力(Paw)、潮气量(VT)、分钟通气量(MV)以及呼末二氧化碳分压(PETCO2);测定T0、T2、T4时点动脉血高铁血红蛋白(MetHb)和亚硝酸根(NO2-/NO3-)水平;处死动物后比较各组肺组织湿/干重比、支气管肺泡灌洗液(BALF)中饱和磷脂/总磷脂(DSPC/TPL)及饱和磷脂,总蛋白(DSPC/TP)、肺表面张力和白细胞计数,并行肺组织损伤评分。结果Ⅲ、Ⅳ、Ⅴ、Ⅵ组BALF中DSPC/TP及肺表面张力较Ⅰ组下降(P<0.05),通气结束时Crs较通气前下降(P<0.05),而Ⅱ组无显著性变化(P>0.05);与通气前比较,各组通气结束时MetHb与:NO2-/NO3-水平无变化,各组BALF中白细胞计数、肺组织损伤评分、肺泡扩张度和湿/干重比之间比较差异无统计学意义。结论1.3MAC异氟醚或七氟醚混合20ppmNO吸入可以安全用     

丙泊酚或七氟醚复合瑞芬太尼对食管癌根治术患者单肺通气时中性粒细胞NF-κB活性的影响

目的 比较丙泊酚或七氟醚复合瑞芬太尼对食管癌根治术患者单肺通气时中性粒细胞NF-κB活性的影响.方法 择期全麻单肺通气下行左侧开胸食管癌根治术患者40例,年龄40 ～ 64岁,性别不限,体重指数18 ～ 25 kg/m2,ASA分级Ⅰ或Ⅱ级.采用随机数字表法,将其分为2组(n=20):丙泊酚-瑞芬太尼组(P组)和七氟醚-瑞芬太尼组(S组).麻醉诱导后气管插管并机械通气,麻醉维持:P组静脉输注丙泊酚4～8 mg·kg-1 ·min-1,S组吸入1% ～3%七氟醚,2组均静脉输注瑞芬太尼0.2μg· kg-1 ·min-1,维持Narcotrend指数值40～ 50,间断静脉注射顺苯磺酸阿曲库铵7 mg维持肌松.分别于气管插管后5 min、单肺通气开始即刻、30、60、90 min、恢复双肺通气即刻、恢复双肺通气后10min及术毕时采集桡动脉血样,进行血气分析,计算氧合指数和呼吸指数,测定血浆IL-1浓度,提取中性粒细胞核蛋白,测定中性粒细胞NF-κB DNA结合活性.结果 与P组比较,S组呼吸指数、血浆IL-1浓度和中性粒细胞NF-κB DNA结合活性升高(P＜0.05),氧合指数差异无统计学意义(P＞0.05).结论 与七氟醚-瑞芬太尼麻醉比较,丙泊酚-瑞芬太尼麻醉可抑制食管癌根治术患者单肺通气时中性粒细胞NF-κB激活,有助于减轻肺组织炎性反应.     

丙泊酚或异氟醚麻醉对单肺通气时氧化应激反应的影响

目的 观察丙泊酚或异氟醚麻醉对单肺通气(OLV)时氧化应激反应的影响.方法 48例择期行食管癌根治术患者,随机分为丙泊酚单肺通气组(Pro-OLV组)、异氟醚单肺通气组(Iso-OLV组)、丙泊酚双肺通气组(Pro-TLV组)和异氟醚双肺通气组(Iso-TLV组),每组12例.于开胸前(T0)、OLV后(TLV组于开胸后)30 min(T1)、90 min(T2)、150 min(T3)、手术结束时(T4)测定血清超氧化物歧化酶(SOD)、丙二醛(MDA)及NO浓度.结果 与T0时比较,OLV组T1～T4时的SOD活性降低,MDA浓度及NO浓度升高(P<0.01),而TLV组无明显变化.与TLV组比较,OLV组T1～T4时的SOD活性降低,MDA及NO浓度升高(P<0.01).结论 丙泊酚或异氟醚麻醉均不能减轻OLV时氧化应激反应.     

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