高频程序通气对心肺复苏呼吸支持作用的临床观察

目的 探讨高频程序控制通气在心肺复苏过程中的应用价值.方法 30例心肺复苏术后无自主呼吸的患者随机分为3组:常规控制通气组(A组)、5∶ 5高频程序控制通气组(B组)及7∶ 3高频程序控制通气组(C组),各组分别采用相应的机械通气模式进行呼吸支持.自主循环恢复开始计时,分别测定0、1、4、12、24 h动脉血氧分压(PaO2)、氧合指数(OI)、动脉二氧化碳分压(PaCO2)、心率(HR)、平均动脉压(MAP)、中心静脉压(CVP)、气道峰压(PIP).结果 ①B、C组PaO2、OI在1、4、12 h均显著高于A组(P<0.01);C组PaO2、OI在4、12、24 h均高于B组(P<0.05).PaCO2各时点组间比较差异无统计学意义(P＞0.05).②各时点B、C组PIP、CVP均低于A组(P＜0.01),B、C组MAP均高于A组(P＜0.05),三组HR比较差异无统计学意义(P＞0.05).结论 高频程序控制通气对心肺复苏患者具有较好的呼吸支持作用,改善氧合快,对血流动力学影响小,不易产生二氧化碳潴留, 使用便捷.两种程序控制通气中,高频与常频通气时间比为7∶ 3的高频程序控制通气模式通气效果更佳.     

大型多功能呼吸机无创通气治疗急性肺损伤临床观察

目的:观察大型多功能呼吸机无创正压通气治疗急性肺损伤的临床疗效。方法:32例急性肺损伤患者随机分为无创组(18例)和有创组(16例),在综合治疗同时,分别给予大型多功能呼吸机无创正压通气和有创通气治疗,观察对比机械通气前、后不同时段的氧合指数、呼吸频率、心率和相关指标。结果:两组治疗后1~2 h和24 h后的氧合指数、呼吸频率、心率均改善,差异无统计学意义(P>0.05);两组成功率分别为72.2%、75.0%,差异无统计学意义(P>0.05)。结论:大型多功能呼吸机无创正压通气治疗急性肺损伤,临床疗效确切,并发症少、患者易接受。     

持续气管内吹气在急性肺损伤幼猪通气中的作用

目的 观察持续气管内吹气联合保护性低通气压控制通气对内毒素诱导急性肺损伤幼猪的疗效.方法 12只上海小白猪,内毒素60 μg,/ks静脉维持诱导肺损伤.随机(随机数字法)分为单纯机械通气组(MV,n=6)和联合气管内吹气组(TGI,n=6).呼吸机设置参数为吸气峰压10cmH2O(1 cmH2O=0.981 kPa);呼吸末正压2 cmH2O;呼吸频率30次/min,吸气时间0.4 s;流速20 L/min.TGI组经留置婴儿胃管给予2 L/min空气吹入,调节呼吸机吸氧浓度使吸入混合气体所测氧浓度为0.4.记录牛命体征、中心静脉压、通气功能和呼吸力学参数及动脉血气分析.结果 急性肺损伤成模后4 h,与MV组比较,TGI组呼气潮气量、通气效率指数显著升高(P<0.01),平均气道阻压下降(P<0.05).动脉血气分析提示TGI组pH值明显纠正,二氧化碳分压显著下降(P<0.01);同时氧分压、氧合指数显著改善(P<0.05).但两组心率、呼吸频率、动脉压、中心静脉压、肺顺应性和平均气道阻力差异均无统计学意义.组织学检查提示TGI组肺组织炎症程度及出血状况明显减轻.结论 持续气管内吹气可以显著提高急性肺损伤机械通气效率,促进二氧化碳排出,并改善氧合能力,在急性肺损伤治疗中具有一定的应用前景.     

脓毒症患者并发急性肺损伤危险因素分析

目的:探讨影响脓毒症患者并发急性肺损伤(ALI)预后的危险因素.方法:回顾性分析入住本院急诊ICU的36例脓毒症并发ALI病例,根据其预后分为存活组(17例)和死亡组(19例),将两组各项指标进行比较,其后选择有意义的变量(P<0.05)进行多因素非条件Logistic 回归分析.结果:单因素分析提示,患者呼吸、平均动脉压、APACHEⅡ评分、急性肺损伤(LIS)评分、住院时间、pH值、氧分压、血乳酸值、氧合指数、既往慢性病史、是否机械通气在脓毒症发生急性肺损伤存活组与死亡组两组间差异具有统计学意义(P<0.05);年龄、体温、心率、二氧化碳分压、性别、感染部位、细菌培养结果两组间差异无统计学意义(P>0.05).多因素 Logistic回归分析提示,APACHEⅡ评分、氧合指数对脓毒症并发ALI预后有显著影响.结论:脓毒症患者并发ALI病死率高,APACHEⅡ评分高、氧合指数低是疾病死亡的危险因素.     

肝素对急性肺损伤/急性呼吸窘迫综合征的治疗作用

研究抗凝治疗对急性肺损伤/急性呼吸窘迫综合征动物模型的治疗作用及其机制。方法将48只大耳白兔随机分为四组:对照组(A组)、内毒素组(B组)、内毒素 肝素组(C组)和内毒素 低分子肝素组(D组),每组12只。肺损伤动物模型采用静脉注射脂多糖来制作,用NovaStstProfileM血气分析仪进行血气分析;用酶联免疫吸附测定(ELISA)法测定肿瘤坏死因子-α(TNF-α);用Westernblots检测磷酸化p38MAPK水平。结果①给予内毒素各组的动脉血氧分压(PaO2)进行性下降,1h后各时间点B、C、D组的PaO2显著低于A组(P<0.05);在4h和6h时,C组和D组PaO2明显高于B组(P<0.05),但C、D组之间差异均无统计学意义。②给予内毒素各组的血浆TNF-α水平进行性升高,在1h后各时间点B、C、D组的血浆TNF-α水平均显著高于A组(P<0.05);在4h和6h时,C组和D组血浆TNF-α水平明显低于B组(P<0.05),C、D组之间差异无统计学意义。③根据肺损伤的病理改变,A、B、C和D组的肺损伤评分分别为0.1分、(2.4±0.5)分、(1.6±0.5)分和(1.8±0.4)分,C、D组的肺损伤评分明显低于B组P<0.05)。④各实验组动物予以内毒素处理1h后p38MAPK的表达较对照组显著升高(P<0.05),C、D组在4h后p38MAPK表达明显低于B组(P<0.05),但C、D组之间差异无统计学意义。结论对于内毒素诱导的ALI动物模型,肝素和LMWH干预可能对ALI有一定的保护作用,表现在改善低氧血症和减轻炎症反应,减轻炎症反应可能与其抑制p38MAPK的活化有关。     

压力和容量控制通气呼吸力学和相关细胞因子的关系

目的研究压力控制通气(PCV)与容量控制通气(VCV)时呼吸力学和血清肿瘤坏死因子-α(TNF-α)及肺表面活性物质蛋白A(SP-A)的关系,进而明确哪种通气模式可以较好的减轻呼吸机相关性肺损伤(VILI)。方法20例需进行机械通气的呼吸衰竭患者随机分成A、B两组,A组先进行PCV12h后,再进行VCV12h。B组与此相反。实验过程中记录心率、血压、呼吸力学指标,分别在通气12h、24h查动脉血气,抽取静脉血测量SP-A及TNF-α浓度。结果A组氧合指数(235.80±31.39)mmHg相对好于B组(199.20±24.91)mmHg,但差异无统计学意义(P>0.05)。A组气道峰压(PIP)(27.90±1.35)cmH2O较B组(33.80±1.48)cmH2O有降低趋势(P<0.05),A组肺顺应性(23.90±8.45)ml/cmH2O较B组(18.39±5.43)ml/cmH2O好(P<0.05)。与B组相比,A组血清中的SP-A(25.25±0.965)μg/ml及TNF-α(0.546±0.063)μg/ml明显偏低(P<0.05)。PIP与血清中SP-A(r=0.386,P<0.05)、TNF-α(r=0.404,P<0.05)之间呈正相关。血清中SP-A与肺顺应性(r=-0.339,P<0.05)、氧合指数(r=-0.393,P<0.05)呈负相关。结论与B组相比,A组降低了PIP、血清中的SP-A及TNF-α的浓度,提示可能降低肺损伤的发生。PIP可能在VILI中起着一定的作用,血清中SP-A浓度的水平,可以作为反映肺损伤程度的生化指标。     

舒氧康对急性肺损伤家兔肺组织肿瘤坏死因子-αmRNA表达的影响

目的:探讨舒氧康对急性肺损伤(ALI)家兔肺组织肿瘤坏死因子-α(TNF-α)mRNA表达的影响及其对肺损伤的治疗作用。方法:将45只家兔随机分为对照组(A组)、肺损伤组(B组)和舒氧康组(C组),每组15只,B和C组采用特制多功能撞击机制成ALI模型,C组经耳缘静脉给予舒氧康静滴[0.3mL/(kg·min)],分别在损伤前及损伤后2、4、6h采血测定TNF-α水平,6h后处死动物,取肺组织测定肺组织TNF-α水平、TNF-αmRNA表达、肺水含量、肺体质量比值及观察病理变化。结果:与A组相比,B组损伤后肺组织及血浆TNF-α水平、肺组织TNF-αmRNA表达显著升高(P<0.05),PaO2显著降低(P<0.05),肺水含量及肺体质量比值显著增高(P<0.05),镜下见肺间质、肺泡水肿,大量炎细胞浸润。C组经舒氧康治疗后,与B组比较,肺组织及血浆TNF-α水平、肺组织TNF-αmRNA表达降低(P<0.05),PaO2明显升高(P<0.05),肺水含量及肺体质量比值减少,肺水肿减轻。结论:舒氧康能抑制ALI家兔肺组织TNF-αmRNA的表达,降低肺组织...更多和血浆TNF-α水平,减轻肺组织的病理损害从而治疗ALI。     

ω-3鱼油脂肪乳剂对内毒素致兔急性肺损伤保护作用机制的研究

目的 探讨ω-3鱼油脂肪乳剂对内毒素(ET)致兔急性肺损伤(ALI)的保护作用.方法 清洁级新西兰兔24只,随机分为对照组(A组)、ET致伤组(B组)、ω-3鱼油脂肪乳剂预处理组(C组).经静脉一次性注射ET复制兔ALI 模型,各组分别于0、0.5、1、2、4 h不同时间点测定呼吸频率、心率、血气分析;4 h点处死动物,测定肺组织TNF-α、髓过氧化酶(MPO)、白细胞介素10(IL-10)含量;取肺组织观察病理变化,并做病理评分、测湿/干质量比值(W/D)及肺含水量.结果与对照组相比,B组心率加快、呼吸急迫;动脉血氧下降,肺组织出现明显病理组织学损伤,W/D、肺含水量升高.TNF-α:B组明显升高,与A、C两组比较差异有统计学意义(P<0.05),C组与A组比较差异无统计学意义(P>0.05).IL-10:B、C两组较A组均升高(P<0.05),C组与B组比较差异无统计学意义.B、C两组MPO较A组均升高,三组差异有统计学意义.C组W/D、肺含水量、肺损伤病理组织评分均低于B组(P<0.05).结论 ω-3鱼油脂肪乳可以减少TNF-α生成,抑制PMN在肺内扣押,并有上调IL-10的趋势,对内毒素致兔ALI具有一定保护作用,但其影响IL-10的具体机制仍需进一步探讨.     

不同剂量乌司他丁对百草枯急性肺损伤大鼠肝肾功能的影响

目的:观察不同剂量乌司他丁(UTI)对百草枯(PQ)急性肺损伤大鼠肝肾功能的影响。方法:将50只SD大鼠随机分为正常对照组(A)、PQ中毒组(B)、小剂量UTI治疗组(C)、中剂量UTI治疗组(D)、大剂量UTI治疗组(E)五组,每组10只。B、C、D、E组大鼠采用PQ一次性灌胃染毒法(80 mg/kg)复制PQ中毒模型,A组采用等量生理盐水灌胃。灌胃30 min后,C组腹腔注射UTI 100 k U/kg,D组腹腔注射UTI 300 k U/kg,E组腹腔注射UTI 600 k U/kg,A、B组注射等量生理盐水。24 h后检测血清ALT、AST、BUN、Cr浓度,光镜下观察肺组织病理学变化,进行肺损伤评分。结果 :C、D、E组和B组比较,大鼠血清ALT、AST、BUN、Cr浓度及肺组织损伤病理评分存在显著差异(P<0.05);C、D、E组之间比较,血清ALT、AST、BUN、Cr浓度无显著差异(P>0.05),肺组织损伤病理评分存在显著差异(P<0.05)。结论:较大剂量UTI对急性PQ中毒大鼠急性肺损伤具有较强保护作用,对肝肾功能无明显影响。     

尾加压素受体拮抗剂对急性肺损伤的干预效应

目的探讨尾加压素受体拮抗剂(urotensin receptor antagonist,URA)对损伤肺的影响。方法健康SPF级Sprague Dawley(SD)大鼠49只,随机分为A、B、C三组:抽取7只注射生理盐水作为正常对照(A组);B、C两组各21只,二组所有大鼠用油酸复制急性肺损伤(acute lung injury,ALI)模型,B组为模型对照组,C组在模型基础上加用URA为干预组。三组均于注射后3h各抽动脉血作血气分析测定血氧分压,A组抽动脉血后全部活杀取肺,B、C两组分别于3(抽动脉血后)及12、24h三个时间段各取7只活杀取肺,右肺称湿重后烘干,左肺立即以中性福尔马林固定作病理切片。结果A组大鼠注射生理盐水后无异常表现,B、C两组注射油酸后均出现呼吸急促、活动减少或不合群、紫绀等表现,与A组相比,B、C两组动脉血氧分压(PaO2)明显下降(P<0.05),肺湿/干(W/D)比值明显升高(P<0.05),但A、B两组间差异无统计学意义(P>0.05)。C组活动能力改善较B组更快,肺组织病理符合急性肺损伤变化,随时间延长,炎症细胞、红细胞、肺水肿进行性加重,但C组红细胞渗出较B组有所减少。结论尾加压素受体拮抗剂可能对急性肺损伤动物肺损害有保护作用。     

内毒素预处理对大鼠急性肺损伤的影响

目的　探讨肺泡巨噬细胞核因子κB( NFκB)活性变化在内毒素所致大鼠急性肺损伤中的作用。方法　 Wistar大鼠 36只 ,12只腹腔连续 3d注射脂多糖 ( L PS) 0 .5、0 .5和 1.0 mg/ kg,第 4 d腹腔注射脂多糖 ( L PS) 6 mg/ kg( L PS预处理组 ) ;12只腹腔注射内毒素 6 m g/ kg(肺损伤组 ) ;12只为正常对照组 ,腹腔注射生理盐水。注射完毕后 4 h处死大鼠 ,取肺测定肺组织湿 /干质量比 ( W/ D) ;以 99Tc标记的血清白蛋白测定肺通透指数 ;从肺灌洗液中提取肺泡巨噬细胞核蛋白 ,用凝胶电泳迁移率 ( EMSA)方法检测 NFκB活性。各组肺进行病理组织学观察。结果　 L PS预处理组肺 W/ D及通透性显著低于肺损伤组 ,而 Pa O2 和碱剩余高于肺损伤组 ;且肺损伤组及 L PS预处理组的 NFκB活性皆显著升高 ( P均 <0 .0 5 ) ,L PS预处理组高于肺损伤组。结论　内毒素预处理可减轻内毒素造成的肺损伤 ,此现象可能与肺泡巨噬细胞 NFκB活性变化有关     

沐舒坦对吸入性肺损伤大鼠的肺保护作用

目的评价预先使用药物沐舒坦对稀盐酸吸入性肺损伤是否具有保护作用,为临床治疗提供理论依据。方法30只健康SD大鼠随机分成3组:A组为生理盐水吸入组;B组为稀盐酸吸入组;C组为稀盐酸吸入加沐舒坦处理组。C组预先以50mg/kg沐舒坦腹腔注射,每日1次,连续3d;A、B两组则以腹腔注射等体积生理盐水代替。第3d腹腔注射沐舒坦或生理盐水30min后,A组以1.2ml/kg(pH5.3)的生理盐水经气管内注入造成非盐酸吸入肺损伤作为对照;B、C组则以1.2ml/kg(pH1.25)的盐酸加生理盐水混合液经气管内注入制备盐酸吸入性肺损伤模型。观察盐酸注入5h后大鼠动脉血气、肺湿/干重比(W/D)以及光镜下肺组织病理改变及肺损伤评分。结果1B、C组动脉血氧分压(PaO2)在盐酸吸入5h时比A组明显降低,B组又低于C组,组间比较差异均有显著性(P均<0.01);但pH和动脉血二氧化碳分压(PaCO2)在3组间差异无显著性(P>0.05)。23组W/D由低到高依次为A组、C组和B组,组间比较差异均有显著性(P均<0.01)。3光镜下组织病理学观察发现,B组肺损伤最为严重,而C组损伤比B组要轻;肺损伤程度评分A组最低,C组较B组低,3组间比较差异有显著性(P<0.05或P<0.01)。结论沐舒坦能减轻稀盐酸吸入所引起弥漫性肺损伤。     

Partial liquid ventilation with FC-77 suppresses the release of lipid mediators in rat acute lung injury model

OBJECTIVE: To investigate whether the release of lipid mediators is suppressed in rats with experimentally induced acute lung injury managed with partial liquid ventilation (PLV) using FC-77. DESIGN: Prospective, randomized controlled study. SETTING: Research laboratory in a university. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: After tracheostomy was performed under general anesthesia, lung injury was induced by intratracheal instillation of HCl. The PLV group was then subjected to conventional gas ventilation for 30 mins, followed by PLV using FC-77. The control group was subjected to conventional gas ventilation throughout the study period. MEASUREMENTS AND MAIN RESULTS: In the PLV group the following results were obtained: a) impaired oxygenation was markedly improved; b) the increase in the serum levels of lipid mediators such as leukotriene B4, thromboxane A2, and 6-keto-prostaglandin F1alpha was suppressed; and c) the increase in the concentrations of leukotriene B4, thromboxane A2, and 6-keto-prostaglandin F1alpha in the total lung homogenate at 180 mins after lung injury was also suppressed. CONCLUSION: This study indicates that PLV using FC-77 suppresses the release of lipid mediators in our rat model of acute lung injury. However, further investigation is needed to clarify the precise mechanism of this effect.     

乌司他丁联合氨溴索治疗胸外伤所致ALI／ARDS的临床研究

目的探讨乌司他丁联合氨溴索在胸外伤所致ALI／ARDS患者中的治疗效果和作用。方法选取60例胸外伤所致ALI／ARDS的患者进行研究,随机分为：A（对照组）、B（氨溴索治疗组）、C（乌司他丁联合氨溴索治疗组）三组。测定各组患者治疗前后PaO2、PaO2／FiO2、血浆IL-6水平变化。结果B组患者各项指标均优于A组,通气24h后C组氧分压及氧合指数较B组改善,IL-6水平较B组降低,且较A组差异有统计学意义。结论氨溴索联合乌司他丁能较好减轻肺损伤程度,改善氧合,较单存使用氨溴索更为有益,两者均是急性肺损伤时的有效治疗药物。     

Hypervolemia induces and potentiates lung damage after recruitment maneuver in a model of sepsis-induced acute lung injury

Introduction

Recruitment maneuvers (RMs) seem to be more effective in extrapulmonary acute lung injury (ALI), caused mainly by sepsis, than in pulmonary ALI. Nevertheless, the maintenance of adequate volemic status is particularly challenging in sepsis. Since the interaction between volemic status and RMs is not well established, we investigated the effects of RMs on lung and distal organs in the presence of hypovolemia, normovolemia, and hypervolemia in a model of extrapulmonary lung injury induced by sepsis.

Methods

ALI was induced by cecal ligation and puncture surgery in 66 Wistar rats. After 48 h, animals were anesthetized, mechanically ventilated and randomly assigned to 3 volemic status (n = 22/group): 1) hypovolemia induced by blood drainage at mean arterial pressure (MAP)≈70 mmHg; 2) normovolemia (MAP≈100 mmHg), and 3) hypervolemia with colloid administration to achieve a MAP≈130 mmHg. In each group, animals were further randomized to be recruited (CPAP = 40 cm H₂O for 40 s) or not (NR) (n = 11/group), followed by 1 h of protective mechanical ventilation. Echocardiography, arterial blood gases, static lung elastance (Est,L), histology (light and electron microscopy), lung wet-to-dry (W/D) ratio, interleukin (IL)-6, IL-1β, caspase-3, type III procollagen (PCIII), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) mRNA expressions in lung tissue, as well as lung and distal organ epithelial cell apoptosis were analyzed.

Results

We observed that: 1) hypervolemia increased lung W/D ratio with impairment of oxygenation and Est,L, and was associated with alveolar and endothelial cell damage and increased IL-6, VCAM-1, and ICAM-1 mRNA expressions; and 2) RM reduced alveolar collapse independent of volemic status. In hypervolemic animals, RM improved oxygenation above the levels observed with the use of positive-end expiratory pressure (PEEP), but increased lung injury and led to higher inflammatory and fibrogenetic responses.

Conclusions

Volemic status should be taken into account during RMs, since in this sepsis-induced ALI model hypervolemia promoted and potentiated lung injury compared to hypo- and normovolemia.     

Ceftazidime improves hemodynamics and oxygenation in ovine smoke inhalation injury and septic shock

OBJECTIVE: To investigate ceftazidime in acute lung injury (ALI) and sepsis. DESIGN AND SETTING: Prospective, randomized, controlled animal study in an investigational ICU at a university hospital. INTERVENTIONS: Eighteen female Merino sheep were prepared for chronic study and subjected to smoke inhalation and septic challenge according to an established protocol. MEASUREMENTS AND RESULTS: Whereas global hemodynamics and oxygenation remained stable in sham animals (no injury, no treatment), the injury contributed to a hypotensive-hyperdynamic circulation in the control group (smoke inhalation and sepsis, no treatment), as indicated by a significant increase in cardiac index) and heart rate and a drop in mean arterial pressure. Treatment with ceftazidime (smoke inhalation and sepsis, treatment group) stabilized cardiac index and heart rate and attenuated the decrease in mean arterial pressure. The deterioration in PaO2/FiO2 ratio and pulmonary shunt fraction (Qs/Qt) was significantly delayed and blunted by ceftazidime. At 24 h after injury a significant increase in airway obstruction scores of bronchi and bronchioles in both injured groups was observed. Ceftazidime significantly reduced airway obstruction vs. control animals. Whereas plasma nitrate/nitrite levels increased similarly in the two injured groups, lung 3-nitrotyrosine content remained at the baseline level in the ceftazidime group. CONCLUSIONS: In ovine lung injury ceftazidime improves global hemodynamics and oxygenation not only by bacterial clearance but also via reduction in toxic nitrogen species such as 3-nitrotyrosine. Therefore ceftazidime appears as a clinically relevant adjunct in the common setting of sepsis-associated lung injury.     

Do lung recruitment maneuvers decrease gastric mucosal perfusion?

Objective To evaluate effects of lung recruitment maneuvers on gastric mucosal perfusion, systemic circulation, and lung mechanics in patients with acute lung injury.Design Prospective observational clinical study.Setting General intensive care unit of university hospital.Patients and participants Fourteen patients with acute lung injury (ten in the main study group and four in a validation group).Interventions Three 2-min-long recruitment maneuvers (RM) with transient increases in mean airway pressure to 35 cmH₂O (RM1 and RM2) and 44 cmH₂O (RM3).Measurements and results Measurements of systemic hemodynamics, gastric mucosal perfusion (laser Doppler flowmetry), and lung mechanics were performed immediately before, at the end of, and 3 min after each RM. Cardiac index decreased during all RMs while mean arterial pressure decreased only during RM3. Gastric mucosal perfusion was not significantly changed during any of the RMs. When comparing values obtained before the first RM with values after the third RM there was a significant decrease in cardiac index (P=0.043) and a non-significant (P=0.051) decrease in gastric mucosal perfusion. There were no significant changes in systemic oxygenation or lung mechanics after three RMs, even though four patients showed marked transient increases in systemic oxygenation during RMs.Conclusions In this study of ten patients there were no significant changes in gastric mucosal perfusion during lung recruitment maneuvers. There was, however, a trend towards gradual decreases in gastric mucosal perfusion.     

米力农吸入对急性肺损伤家兔肺iNOS和eNOS表达的影响

目的:观察米力农吸入对急性肺损伤(ALI)家兔肺iNOS和eNOS表达的影响并探讨其保护机制。方法:将45只家兔随机分为对照组(A组),肺损伤组(B组)和米力农吸入组(C组),每组15只,B和C组采用特制多功能撞击机制成急性肺损伤模型,C组经气管给予米力农雾化吸入,分别在0、1、2、3、4h时间点行血气分析,4h后处死动物,测定肺湿干比(W/D)、血清NO、肺组织丙二醛(MDA)和髓过氧化物酶(MPO)含量,免疫组化法检测肺组织iNOS和eNOS表达。结果:与A组相比,B组损伤后PaO2、SaO2显著降低(P<0.05),肺iNOS表达显著增强,eNOS表达明显降低(P<0.05),肺W/D、血清NO、肺MDA和MPO含量显著增高(P<0.05)。C组米力农吸入后,与B组比较,PaO2、SaO2明显升高(P<0.05),肺iNOS表达显著降低,eNOS表达明显升高(P<0.05),肺W/D、血清NO、肺MDA和MPO含量明显降低(P<0.05)。结论:米力农通过抑制肺iNOS异常高表达和增加eNOS表达对急性肺损伤有保护作用。     

巨噬细胞在急性肺损伤中的作用

目的 通过观察急性肺损伤中炎细胞的变化规律。阐明炎细胞在急性肺损伤中的作用。方法 采用20%Ⅲ度体表烧伤复合一次性腹腔内毒素（1mg/kg)注射为实验动物模型。并分别以单纯烧伤，单纯内毒素注射，生理盐水注射为对照组，观察伤后肺组织的病理变化，支气管肺泡灌洗液（BALF）中的细胞总数及中性粒细胞（PMN）分类计数。结果 单烧组和单注组BALF细胞总数明显高于正常对照组，主要是巨噬细胞（Mφ）增加，而烧注组BALF细胞总数除1.5h外无明显升高，1.5h时PMN比例却明显增加，烧注组肺病理改变比单烧组，单烧组明显加重，以伤后1.5h最为显著，结论 PMN是内毒素血症急性肺损伤的主要效应细胞，而Mφ则对急性肺损伤可能有某种保护作用。     

不同时间单肺通气后兔两侧肺损伤程度比较

目的观察不同长度时间单肺通气后,两侧肺的氧合指数、肺损伤评分及湿/干质量比的变化。方法24只日本大耳白兔随机分为4组各6只。对照组(C组)双肺通气2h;O1组、O2组及O3组为单肺通气组,采用自制双腔气管导管建立单肺通气模型后,分别单肺通气1、2、3h,随后恢复双肺通气1h。在实验结束前开胸,分别由两侧肺静脉同时抽取肺静脉血、由股动脉抽取动脉血做血气分析测定氧合指数。实验结束后处死动物测肺组织湿/干质量比并做肺组织病理切片行肺损伤评分。结果肺损伤评分C组左右侧相比较差异无统计学意义(P>0.05),另三组组内左右侧比较左侧明显增高(P<0.01);各组间右侧比较表现为逐步升高,其中O3组最明显;各组间左侧相比较亦表现为逐步升高。肺组织湿/干质量比及氧合指数的变化与之相对应。结论长时间单肺通气可以导致急性肺损伤,这种损伤是不均一性的,损伤的程度与单肺通气时间相关,且非通气侧肺要比通气侧肺损伤严重。