地塞米松对重症胎粪吸入幼兔肺组织中肿瘤坏死因子α和白介素8水平的影响

目的探讨地塞米松对胎粪吸入幼兔肺组织中肿瘤坏死因子-α(TNF-α)和白介素-8(IL-8)水平的影响。方法将24只日龄20～30天的幼兔随机分为对照组、生理盐水组和地塞米松组各8只,对照组气管插管后不灌胎粪;后两组气管插管后注入4 ml/kg的45 mg/ml胎粪混合物,地塞米松组在胎粪灌入后1 h和3 h静脉注射地塞米松0.5 mg/kg,生理盐水组在同样时间静脉注射等量的生理盐水;3组均在呼吸机比例辅助通气模式下通气,维持潮气量4～6 ml/kg、血氧饱和度85%以上和呼气末二氧化碳分压35～45 mm Hg为目标调节呼吸机参数,8 h后处死。取肺组织匀浆和支气管肺泡灌洗液(BALF),并用酶联免疫吸附试验测定TFN-α和IL-8的含量。结果对照组BALF和肺组织匀浆中TNF-α、IL-8含量均低于地塞米松组和生理盐水组,地塞米松组低于生理盐水组[BALF中TNF-α(pg/ml):(29.2±2.0)、(47.8±3.8)、(59.2±4.4),IL-8(pg/ml):(297.4±10.9)、(444.3±48.6)、(596.1±90.8);肺组织匀浆中TNF-α:(40.2±2.3)、(57.4±6.2)、(76.2±7.7),IL-8:(187.9±11.0)、(485.3±30.2)、(645.0±13.7)],差异有统计学意义(P均<0.05)。结论地塞米可以降低幼兔胎粪吸入肺组织匀浆和BALF中TNF-α和IL-8的水平,减轻肺损伤。     

细胞间黏附分子-1在胎粪诱导的新生大鼠急性肺损伤中的作用

目的探讨细胞间黏附因子-1(ICAM-1)在胎粪吸入性急性肺损伤中的作用。方法将20只新生SD大鼠随机均分为胎粪模型组和对照组。胎粪模型组复制胎粪吸入性急性肺损伤模型,行气管插管术,胎粪模型组新生大鼠经气管注入2.0 mL.kg-1胎粪;对照组新生大鼠经气管注入2.0 mL.kg-19 g.L-1盐水,其余手术操作2组相同。术后60 min拔管,逐层缝合手术创面,观察24 h后处死动物,取肺,取支气管肺泡灌洗液5 mL备镜下白细胞计数,取肺右下叶分为2份,一份行免疫组织化学分析,一份采用比色法测肺组织髓过氧化物酶活性。结果 ICAM-1在胎粪模型组新生大鼠肺组织中的表达高于对照组(t=21.142,P<0.001);胎粪模型组新生大鼠肺组织髓过氧化物酶活性高于对照组(t=13.621,P<0.001);胎粪模型组新生大鼠支气管肺泡灌洗液白细胞计数高于对照组(t=10.714,P<0.001)。结论内皮细胞释放ICAM-1增多,引起白细胞释放反应,导致炎性反应失衡,可能在胎粪吸入性急性肺损伤中起重要作用。     

NF-κB抑制剂在新生儿机械通气肺损伤中的作用研究

目的 探讨NF-κB抑制剂吡咯烷二硫代氨基甲酸盐(PDTC)对机械通气肺损伤的保护作用及其作用机制.方法 20只3周左右日龄的普通级健康幼兔,随机分为4组.①机械通气组,VT=24 ml/kg;②机械通气+PDTC组,机械通气前半小时耳缘静脉注射PDTC 100 mg/kg,VT=24 ml/kg;③复合损伤组,气管内滴入脂多糖(LPS)0.1 mg/kg,然后进行机械通气,VT=24 ml/kg;④复合损伤+PDTC组,耳缘静脉注射PDTC 100 mg/kg,半小时后气管内滴入LPS 0.1 mg/kg,然后进行机械通气,VT=24 mL/kg.持续通气4 h.检测肺组织髓过氧化物酶(MPO)、NF-κB活性与肺组织匀浆中TN-αmRNA和IL-8 mRNA的表达和蛋白含量,并观察肺组织病理改变.结果 PDTC能显著减轻机械通气和机械通气复合内毒素肺损伤的病理改变,干预组MPO、NF-κB活性、TNF-α和IL-8蛋白和基因表达均低于相应的未用PDTC干预组(P<0.01).结论 PDTC可能通过抑制NF-κB的活化,减少致炎细胞因子基因转录与蛋白表达、释放,减轻炎细胞浸润,从而对机械通气和机械通气复合内毒素肺损伤起到一定的保护作用.     

幼兔胎粪吸入性肺损伤后支气管肺泡灌洗液中肿瘤坏死因子水平及其意义

目的　研究 TNFα在幼兔胎粪吸入后 BALF中的动态变化。方法 :1 )通过气管内灌入胎粪 0 .6 ml/kg和 4ml/kg建立轻、重度幼兔胎粪吸入模型 ;2 )应用放射免疫法检测 BALF中 TNFα含量。结果 :1 )胎粪吸入可引起肺炎症反应 ,表现 BAL F中白细胞数和 PMN增加 ,胎粪吸入后 2 4小时达高峰 ,72小时基本恢复正常 ;2 )胎粪吸入后 BALF中 TNFα含量明显升高 ,1 6～ 2 4小时达高峰 ,72小时接近正常 ,且上述改变於重度胎粪吸入组与轻度胎粪吸入组比较有极显著性差异。与 PMN做相关分析 ,具有明显的相关性。结论 :1 )幼兔胎粪吸入后 ,肺产生明显的炎症反应 ;2 ) TNF。参与胎粪吸入性肺损伤发生发展。     

卡托普利在高氧致新生大鼠肺损伤模型中的保护作用

目的：观察卡托普利对高氧暴露新生大鼠支气管肺泡灌洗液(BALF)及肺组织形态学改变的影响。方法：足月新生Wistar大鼠40只生后即置于有机玻璃氧舱内持续吸入高浓度氧(FiO2=0.90)14d、21d造成高氧肺损伤模型,治疗组经胃管灌服卡托普利每日60mg/kg(用生理盐水配成5.4mg/mL混悬液),对照组每天经胃管灌服等量生理盐水,空气对照组:吸入空气(FiO2=0.21)。对4组大鼠进行肺系数、BALF中蛋白含量及BALF细胞计数和分类测定并同步观察肺组织形态学的改变。结果：模型组及盐水对照组14d,21d肺系数、BALF中蛋白含量、BALF细胞总数、中性粒细胞、淋巴细胞和嗜酸性粒细胞比例较空气对照组显著升高(P<0.01)。卡托普利治疗组与模型组比较上述指标(除淋巴细胞外)均显著下降(P<0.05或P<0.01);与空气对照组比较亦有统计学差异,P<0.05。模型组及盐水对照组14d,21d肺组织学表现为不同程度的肺泡炎、肺泡间隔增宽、肺泡融合、肺泡数量减少;而卡托普利治疗组肺组织病变明显减轻。结论：卡托普利对高氧所致肺损伤具有一定的保护作用。     

幼兔胎粪吸入性肺损伤后支气管肺泡灌洗液中肿瘤坏死因子水平及其意义

目的研究TNF。在幼兔胎粪吸入后BALF中的动态变化。方法1)通过气管内灌入胎粪．0．6ml／kg和4ml／kg建立轻、重度幼兔胎粪吸入模型;2)应用放射免疫法检测BALF中TNF。含量。结果1)胎粪吸入可引起肺炎症反应,表现BALF中白细胞数和PMN增加,胎粪吸入后24小时达高峰,72小时基本恢复正常;2)胎粪吸入后BALF中TNF     

地塞米松对高氧肺损伤新生大鼠肺水通道蛋白1表达的影响

目的 探讨地塞米松对新生大鼠高氧肺损伤时水通道蛋白1(AQP1)表达的影响及其对肺损伤的可能保护机制.方法 新生Wistar大鼠32只随机分为空气组、高氧组、空气+地塞米松组、高氧+地塞米松组.第3天取肺组织,采用逆转录-聚合酶链反应(RT-PCR)和免疫组织化学法检测AQP1的mRNA表达和分布变化;并对肺湿/干重比(W/D)、支气管肺泡灌洗液(BALF)中的蛋白含量、肺通透指数及组织病理学改变进行对比分析.结果 高氧暴露第3天肺组织出现出血、炎性细胞浸润和水肿,肺W/D、BALF蛋白含量、肺通透指数明显升高;地塞米松干预组肺损伤程度减轻,测定值降低.空气组、高氧组、高氧+地塞米松组AQP1 mRNA相对吸光度比值分别为0.70±0.04、0.42±0.03、1.04±0.04,各组间差异有显著性(P<0.05);与空气组相比,高氧组AQP1 mRNA表达明显降低,高氧+地塞米松组AQP1 mRNA表达显著上调;AQP1蛋白表达与其mRNA变化一致.结论 高氧肺损伤时大鼠肺AQP1表达下调;地塞米松干预对肺损伤有保护作用,上调肺AQP1的表达可能是其作用机制之一.     

分泌型白细胞蛋白酶抑制剂对急性肺损伤新生大鼠肺组织中TNF-α表达的影响

目的研究分泌型白细胞蛋白酶抑制剂(SLPI)在新生大鼠急性肺损伤模型中的抗炎作用。方法利用脂多糖(LPS)气管内滴入制备新生大鼠急性肺损伤的模型;设立SLPI治疗组、LPS组、生理盐水对照组和正常对照组。SLPI治疗组在气管内滴入LPS前预先滴入400μgSLPI。4h后取肺组织匀浆,用ELISA法检测TNF-α的含量。结果SLPI组的肺组织中TNF-α含量(2798·6±618·5)ng/ml,显著低于LPS组(4579·4±357·4)ng/ml,P<0·05。结论在新生大鼠急性肺损伤模型中,SLPI能抑制LPS诱导的TNF-α表达。     

前列腺素 E-1 对新生大鼠高氧肺损伤的作用及机制

目的探讨前列腺素E1(PGE-1)皮下注射对新生大鼠高氧肺损伤的治疗及机制。方法 45只新生Wistar大鼠随机分为对照组、高氧肺损伤模型组、高氧肺损伤+PGE-1组,每组15只。高氧肺损伤模型组、高氧肺损伤+PDE-1组置于氧浓度85%的实验舱内制作高氧肺损伤模型,对照组置于同气压下的空气中。对照组、高氧肺损伤模型组从生后第1天起皮下注射0.9%的Na Cl溶液,高氧肺损伤PGE-1组注射2μg/(kg·d)的PGE-1,均连续注射7天。观察肺干湿质量比,计数肺泡灌洗液(BALF)白细胞总数,HE染色观察支气管及肺泡的形态改变,核染色结合TUNEL查看肺组织凋亡,Western blotting法检测肺组织GRP 78、CHOP蛋白表达。结果对照组、高氧肺损伤模型组和高氧肺损伤+PGE-1组之间肺干湿质量比,BALF白细胞总数,细胞凋亡指数,肺组织GRP78、CHOP蛋白表达的差异均有统计学意义(P0.001),其中高氧肺损伤模型组上述指标最高,高氧肺损伤+PGE-1组居中,对照组最低,两两比较差异均有统计学意义(P0.05)。肺组织病理切片观察见高氧肺损伤模型组肺泡腔增大、融合,间质细胞水肿,可见纤维渗出;高氧肺损伤+PGE-1组介于高氧肺损伤模型组和对照组之间。结论 PGE-1皮下注射对新生大鼠高氧肺损伤有治疗作用,其机制可能与抑制CHOP、GRP 78蛋白表达有关。     

糖皮质激素对高氧诱导新生大鼠肺组织RAGE-NF-κB通路的影响

目的探讨RAGE-NF-κB信号通路在新生大鼠高氧肺损伤过程中的变化,以及糖皮质激素对其的影响。方法 24只新生大鼠随机分为空气对照组、高氧模型组和激素干预组。模型组新生大鼠于生后即暴露于95%氧气浓度环境中1周,空气对照组大鼠生后仅暴露于同室内空气中饲养7 d,激素干预组于造模后行尾静脉注射地塞米松(1 mg/kg),隔天1次,共3次。日龄13 d时处死全部大鼠,RT-PCR检测各组肺组织RAGE m RNA及NF-κB m RNA的表达;Western blot检测RAGE及NF-κB蛋白水平;ELISA法检测血清及肺泡灌洗液(BALF)中TNF-α和s RAGE含量;苏木精-伊红染色后行肺组织病理学评估。结果与对照组和激素干预组相比,高氧模型组肺组织RAGE、NF-κB的m RNA和蛋白表达水平均明显增高(均P0.05),血清中s RAGE含量明显升高(P0.01),BALF中s RAGE含量下降(P0.01);与对照组相比,激素干预组肺组织RAGE、NF-κB的m RNA和蛋白表达水平明显升高(P0.05),血清中s RAGE含量明显升高(P0.05),而BALF中s RAGE含量明显下降(P0.05)。结论 RAGE-NF-κB通路在高氧诱导的新生大鼠肺损伤中活化增强,糖皮质激素可能通过下调RAGE-NF-κB信号通路对高氧肺损伤发挥保护作用。     

地塞米松对脂多糖诱导的急性肺损伤幼鼠肺表面活性物质蛋白－D的影响

目的：肺表面活性物质蛋白D(SP－D)被认为是急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)有价值的生物指标。该研究旨在探讨幼鼠ALI时及地塞米松干预后肺组织SP－D的变化。方法：144只SD大鼠被随机分为正常对照组、肺损伤组和地塞米松治疗组。腹腔内注射脂多糖（LPS，4 mg/kg)建立急性肺损伤模型, 正常对照组注射等量生理盐水, 治疗组于注射LPS 1小时后注射地塞米松(5 mg/kg)。LPS注射后6，12，24，36，48，72 h 每组各处死8只大鼠。用Western blot方法测定肺组织SP－D的相对含量。结果：与正常对照组相比,ALI组在注射LPS后36，48，72 h SP－D含量明显下降(P<0.01)，在48 hrs达最低点(0.92±0.11 vs 3.27±0.52)。地塞米松治疗组于注射LPS后36，48，72 h SP－D含量明显高于ALI组 (P<0.01), 6，12，24，36和48 h 与对照组相比差异无显著性, 72 h差异有显著性(P<0.05)。结论：急性肺损伤早期幼鼠肺组织SP－D含量降低。早期应用地塞米松能使ALI肺组织下降的SP－D明显上升。［中国当代儿科杂志，2007，9（2）：155-158］     

Bronchoalveolar lavage with pulmonary surfactant/dextran mixture improves meconium clearance and lung functions in experimental meconium aspiration syndrome

Surfactant lung lavage is a promising approach in the treatment of meconium aspiration syndrome (MAS). We hypothesise that the enrichment of modified natural surfactant with dextran will enhance meconium clearance from the airspaces during lung lavage and improve lung function in experimental MAS. Human meconium (30 mg/ml; 4 ml/kg) was instilled into the tracheal cannula of anaesthetised and paralysed adult rabbits to induce respiratory failure. The animals were then lavaged with saline (Sal), surfactant without (Surf) and with dextran (Surf+dex). Lung lavage (10 ml/kg in three portions) was performed with diluted surfactant (Curosurf(R), 10 mg/ml, 100 mg/kg) without or with dextran (3 mg/mg of surfactant phospholipids) or saline and the animals were conventionally ventilated with 100% O(2) for an additional hour. Lung functions were measured prior to and after meconium instillation, and 10, 30 and 60 min after lavage. The recovery of meconium in bronchoalveolar lavage (BAL) fluid was quantified. More meconium solids was recovered in the surfactant-lavaged than in the saline-lavaged groups (Surf: 12.4 +/- 3.9% and Surf+dex: 17.5 +/- 3.5% vs. Sal: 4.8 +/- 1.0%; both P < 0.01). Moreover, more meconium solids was obtained by Curosurf/dextran than by Curosurf-only lavage (P < 0.05). In the Surf group, the values for PaO(2)/FiO(2) were significantly higher than in the controls (at 60 min: 24.5 +/- 4.2 kPa vs.9.1 +/- 2.2 kPa, P < 0.01). An additional increase in oxygenation was seen in the Surf+dex group (at 60 min: 34.2 +/- 8.1 kPa, P vs. Surf group <0.01). The lung-thorax compliance was higher in the Surf+dex group in comparison with the Sal and Surf groups (at 60 min: 9.6 +/- 0.9 vs.7.6 +/- 1.2, P < 0.01 and 8.0 +/- 0.7 ml/kPa/kg, P < 0.05). The enrichment of Curosurf with dextran improves meconium clearance and lung functions in surfactant-lavaged rabbits with meconium aspiration.     

Perfluorochemical liquids enhance delivery of superoxide dismutase to the lungs of juvenile rabbits

Previous studies suggest acute lung injury (ALI) in premature newborns is associated with relative deficiency of antioxidant enzymes that may be ameliorated by recombinant human superoxide dismutase (rhSOD). Perfluorochemicals (PFCs) are distributed homogeneously and support gas exchange in diseased lungs. We investigated whether PFCs could provide an effective delivery system for rhSOD. Juvenile rabbits were lung-lavaged, treated with surfactant, and randomized: group I: fluorescently labeled rhSOD (5 mg/kg in 2 mL/kg saline); group II: fluorescently labeled rhSOD (5 mg/kg in 18 mL/kg PFC). Animals were ventilated with oxygen for 4 h; the lungs were harvested for analysis of SOD distribution and oxidative injury. Cardiopulmonary indices remained stable and similar between groups. Qualitative assessment (QA) showed a more homogeneous lung SOD distribution in group II and a better histologic profile. QA of lung SOD distribution showed significant increase in SOD concentrations in group II (7.37 +/- 1.54 microg/mg protein) compared with group I (1.65 +/- 0.23 microg/mg protein). Oxidative injury as assessed by normalized protein carbonyl was 149.1 +/- 26.8% SEM in group II compared with 200.5 +/- 7.3% SEM in group I. Plasma SOD was significantly higher in group II. Administration of rhSOD with or without PFCs does not compromise cardiovascular function or impede lung recovery after ALI. PFCs enhance rhSOD delivery to the lungs by 400% while decreasing lung oxidative damage by 25% compared with rhSOD alone. These data suggest that PFCs optimize lung rhSOD delivery and might enhance the beneficial effects of rhSOD in preventing acute and chronic lung injury.     

实验性胎粪吸入性肺炎一氧化氮吸入干预的研究

目的探讨在不同氧浓度下吸入CD11b不同浓度一氧化氮(nitric oxide, NO)对实验性胎粪吸入性肺炎肺损伤及肺中性粒细胞表面粘附分子CD11b表达的影响,为对该病是否适宜早期NO吸入干预提供实验室依据.方法建立胎粪吸入性肺炎模型兔,对常频机械通气下的胎粪吸入性肺炎家兔在21%或100%的氧浓度下分别给予6×10-6、10×10-6、20×10-6的NO干预12 h,通过图像分析处理测量肺泡间隔平均距离,病理切片检查评估肺损伤程度;测定肺组织髓过氧化物酶(myeloperoxidase, MPO)活性,并采用流式细胞术检测肺泡灌洗液中性粒细胞表面粘附分子CD11b的表达.结果在相同氧浓度下,NO吸入能显著改善氧合.病理结果表明,各干预组和非干预组均可见严重的中性粒细胞浸润到肺间质,轻到中度的肺出血、肺水肿、肺透明膜形成以及中性粒细胞移行到肺泡腔,各吸入NO干预组上述病理变化均有减轻趋势.相同氧浓度下10×10-6、20×10-6的NO 吸入干预组肺MPO活性分别显著低于非干预组(P均<0.05);100%氧浓度下20×10-6NO干预组MPO活性显著低于21%氧浓度下同一NO干预组[(1.4±0.3) U/g vs (2.0±0.1) U/g,P<0.05].在21%或100%氧浓度下,10×10-6、20×10-6NO干预组与非干预组间肺泡灌洗液中性粒细胞CD11b的表达(平均荧光强度)差异显著,表现为NO吸入后CD11b表达显著降低(P均<0.05);在不同氧浓度下同一NO浓度干预组之间差异均无显著意义.各组肺泡间隔距离及肺湿/干重比、平均动脉压差异无显著意义,高铁血红蛋白含量在正常范围之内. 结论 NO吸入可以通过抑制肺组织中性粒细胞粘附分子CD11b的表达而减轻中性粒细胞在肺组织的扣留及MPO的活性,起到潜在的抗炎作用.对胎粪吸入性肺炎,早期吸入NO进行干预可望减轻肺损伤,其合适的NO吸入浓度可能是(10～20)×10-6.     

硫化氢对大鼠高肺血流性肺血管重构机制影响的研究

目的 探讨硫化氢（hydrogen sulfide,H2S）对大鼠高肺血流性肺血管重构的影响及其机制。方法 雄性SD大鼠32只,随机分为分流组、分流＋硫氢化钠（sodiumhydrosulfide,NaHS）组、对照组和对照＋NaHS组。分流组和分流＋NaHS组大鼠经腹主动脉一下腔静脉穿刺建立高肺血流动物模型。用敏感硫电极法测定大鼠肺组织H2S含量;计算大鼠肺肌型动脉（muscularized artery,MA）的百分比及MA的相对中膜厚度（relativemedialthickness,RMT）;应用蛋白质免疫印迹技术（Westernblot）定量分析大鼠肺动脉平滑肌细胞增殖细胞核抗原（proliferation cell nuclear antigen．PCNA）、细胞外信号调节激酶（extracellular signal-regulated kinase,ERKl）、磷酸化细胞外信号调节激酶（phosphorylation extracellular signal-regulated kinase,P-ERK）;应用免疫组织化学法对PCNA进行定位及半定量分析。结果 分流11周后,与对照组比较,分流组大鼠肺组织H2S含量降低（P〈0．05）、肺动脉MA百分比及RMT升高（P〈0．05）;肺动脉PCNA阳性百分比、P-ERK／ERK1增高（P均〈0．01）。与分流组比较,分流＋NaHS组MA百分比及RMT低于分流组（P〈0．01）;肺动脉PCNA阳性百分比、肺动脉P-ERK／ERK1低于分流组（P〈0．01）。结论 H2S通过丝裂原活化蛋白激酶（mitogen-activated protein kinase,MAPK）／ERK信号转导通路调节大鼠高肺血流性肺血管重构。     

Effects of different doses of hydrocortisone on acute lung injury in rats with early septic shock induced by Escherichia coli

OBJECTIVE: To observe the effects of different doses of hydrocortisone (HC) on acute lung injury (ALI) and inflammatory response in rats at early stage of septic shock induced by Escherichia coli and to investigate the possible mechanisms for such differences. METHODS: ALI model of early septic shock was induced in rats by two injections of Escherichia coli at 5 hours interval, with the first intraperitoneal injection of 6.50 x 10(10) cfu/kg and followed by an external jugular vein injection of 2.00 x 10(11) cfu/kg. Forty Wistar rats were randomly divided into the following five groups: normal control, ALI without HC treatment, high-dose HC (150 mg/kg), medium-dose HC (20 mg/kg) and low-dose HC (6 mg/kg). Two hours after the treatment, the specimens were collected for histopathological examination and the biological indexes of lung injury were measured. The expressions of intercellular adhesion molecule-1 (ICAM-1) and glucocorticoid receptor (GR) in lung tissues were also investigated by immunohistochemical assays. RESULTS: The biological indexes of lung injury [wet/dry weight ratio (g/g), total protein concentration in bronchoalveolar lavage fluid (mg/L) and lung permeability index (10(-3))] in ALI group (4.76 +/- 0.10, 278.96 +/- 60.45, 4.73 +/- 0.60) were significantly increased as compared to those in normal control group (4.10 +/- 0.07, 67.46 +/- 13.27, 1.12 +/- 0.15) (P < 0.05). The grades of ALI pathologic changes in ALI group (11.13 +/- 1.13) was significantly higher than that in the normal control group (0.50 +/- 0.53, P < 0.05). The ratio of expression area of ICAM-1 in ALI group (0.149 +/- 0.037) was significantly increased as compared to that in the normal control group (0.051 +/- 0.018) (P < 0.05). The ratio of expression area of GR all group (0.043 +/- 0.037) was significantly decreased as compared to that in the normal Control group (0.124 +/- 9.040) (P < 0.05) After administration of HC, all the lung injury indexes, pathological grades and the ratios of expression area of ICAM-1 and GR were significantly improved, with the most remarkable effects observed in the low-dose HC group. The expressions of ICAM-1 and GR showed a significantly negative linear correlation (r = 0.55, P < 0.0001). CONCLUSION: These results indicated that the low-dose HC treatment had the most remarkable effects of improving the biological indexes of lung injury, inflammatory mediators and pathological changes. These HC dose dependent therapeutic effects might be associated with the level of GR expression.     

Effect of hemocoagulase for prevention of pulmonary hemorrhage in critical newborns on mechanical ventilation: a randomized controlled trial

OBJECTIVE: To investigate the role of hemocoagulase to prevent pulmonary hemorrhage in critical newborns on mechanical ventilation. DESIGN: Randomized controlled trial. SETTING: Neonatal Intensive Care Unit of an affiliated hospital of a Medical University. CHILDREN: Seventy-two critical newborn infants on mechanical ventilation. INTERVENTION: The involved neonates were divided randomly into two groups. Forty-one patients were treated with prophylactic hemocoagulase(dripped through the endotracheal tube), and other 31 neonates served as controls. OUTCOME MEASURES: Incidence of pulmonary hemorrhage, time of ceasing pulmonary hemorrhage if occurred, time of withdrawing of mechanical ventilation in the survivors, and mortality. RESULTS: The incidence of pulmonary hemorrhage (12% vs 42%) and the time of ceasing pulmonary hemorrhage (1.36 +/- 0.65 vs 3.58 +/- 0.82, days), were significantly less in infants treated with prophylactic hemocoagulase as compared with the controls (P<0.05). The time to withdrawal of mechanical ventilation was less in the intervention group (3.20 +/- 0.45 vs 5.04 +/- 1.51 days) (P < 0.05). The mortality in children who received hemocoagulase was 22.0%, which was significantly less than controls (41.9 %) (P < 0.05). CONCLUSION: Prophylactic use of hemocoagulase in mechanically ventilated neonates is effective against pulmonary hemorrhage.     

肺内源性急性肺损伤大鼠肾上腺皮质功能的变化和意义

目的探讨大肠杆菌导致的肺内源性急性肺损伤(ALI)模型大鼠肾上腺皮质功能的变化。方法Wistar大鼠气管注射3ml/kg大肠杆菌混悬液[(4.4～5.6)×1012CFU/L],制作大鼠肺内源性ALI/急性呼吸窘迫综合征(ARDS)模型,存活大鼠随机分为三组,于滴入大肠杆菌混悬液术后6h(n=10)、24h(n=10)、36h(n=10)3个时间点进行观察。每个时间点各8只大鼠作为对照(NS组,气管注射0.9%盐水3mL/kg)。各组分别于术后6、24、36h3个时间点经气管切开插管机械通气,颈总动脉插管监测其血压、血气,取血,PaO2/FiO2<300mmHg(39.9kPa)为ALI,PaO2/FiO2<200mmHg(26.6kPa)为ARDS,符合上述标准的模型大鼠纳入实验。给予小剂量ACTH作ACTH刺激试验,应用ELISA法测定血清中皮质酮、ACTH含量。结果血浆ACTH水平在模型组大鼠各时间点均高于对照组(P均<0.01),24h达峰值(P<0.01)。模型组6h、24h时间点皮质酮较对照组明显升高(P<0.01,P<0.05),36h模型大鼠皮质酮低于对照组(P<0.05)。模型组6h皮质酮达...     

部分液体通气对胎粪性急性肺损伤的病理学影响

目的 通过研究部分液体通气(PLV)对胎粪性急性肺损伤病理学变化的影响,探讨PLV对治疗胎粪性急性肺损伤的效果.方法 68只健康新西兰兔随机分6组,用20%健康新生儿胎粪混悬液3 mL/kg造模,再行机械通气.使用PLV组:全氟化碳(PFC)按3 ml/kg注入兔肺内,再机械通气.造模后6 h处死动物,取兔肺进行病理学检查和评分.结果相对于常频组(3.0±0),常频(PLV)组(2.4±0.6)和高频(PLV)组(2.4±0.6)可以明显降低炎性细胞浸润(P＜0.01),且高频组(2.1±0.3)也有类似作用(P＜0.05).只有高频(PLV)组(1.0±0.7)的肺水肿情况好于常频组(2.0±0.8)(P＜0.01).常频组(2.6±0.5)较容易出现小气道损伤,常频(PLV)组(1.1±0.4)和高频(PLV)组(0.9±0.3)的小气道损伤则不明显(P＜0.01).未发现PLV对肺出血有效.相对于常频组和高频组,使用PLY二组的死亡率较低(21.4%/14.3%).结论 PLV可以明显减轻胎粪性急性肺损伤,并对降低死亡率有一定作用,因而PLV具有临床应用的良好前景.英文作者简介:ZHU Jian-xing (Email:jxzhu.my265@yahoo.com.cn)