经纤维支气管镜确诊儿童肺曲霉病1例

患儿女，17个月，以“喘息58d，间断发热53d，咳嗽21d”为主诉入院。患儿58d前因喘息、气促就诊于当地医院，X线胸片示支气管肺炎，遂于当地医院住院治疗。期间患儿出现发热、咳嗽，并因喘息加重、呼吸困难及心衰转入ICU辅助通气，带机11d撤机。出现气胸1次，行胸腔闭式引流术后缓解。     

急性肺损伤幼鼠肺泡Ⅱ型上皮细胞和SP-A变化相关性的研究

目的：该实验旨在研究急性肺损伤（ALI）时肺泡Ⅱ型上皮细胞（AEC-Ⅱ）超微结构变化和肺组织表面活性蛋白SP-A含量的变化关系，从而探讨ALI的发病机制。方法：48只Sprague-Dawley幼鼠被随机分为正常对照组和ALI组。 腹腔注射脂多糖（LPS，4 mg/kg）建立ALI模型，正常对照组注射等量生理盐水。 LPS注射后24，48，72 h每亚组各处死8只大鼠。 取左肺下肺组织待透射电镜检查。 用Western blot方法测定肺组织SP-A的相对含量。结果：ALI 24 h时，AEC-Ⅱ微绒毛消失。24 h及48 h时板层小体（lamellar body, Lb）数量增加，体积增大，密度减低，排空明显增强，呈指环状绕核排列，细胞增生活跃，代谢旺盛。48 h时Lb呈巨大空泡样变性。肺组织SP-A含量明显高于对照组（24 h时ALI组为6.52±0.62，对照组为5.02±0.35， P< 0.01；48 h时ALI组为6.65±0.62，对照组为5.01±0.36，P< 0.01）。72 h时Lb破溃，数目明显减少，细胞核形态不规则，部分核边界不清，肺组织SP-A含量下降(ALI组为3.87±0.50，对照组为5.22±0.36，P<0.01)。结论： LPS致幼鼠ALI时AEC-Ⅱ和肺组织SP-A的变化为时间依赖性，随AEC-Ⅱ损伤程度的加重肺组织SP-A由代偿转为失代偿，可能是发生ARDS的重要机制之一。     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

6～14岁健康儿童呼出气体一氧化氮水平及其与肺功能的相关性

目的探讨沈阳地区6～14岁健康儿童呼出气体一氧化氮(FeNO)水平与其年龄、身高、体质量、体质量指数(BMI)及肺功能各参数之间的相关性。方法随机测定沈阳地区200名6～14岁健康儿童(男102名,女98名)FeNO水平及其肺功能,采用SAS 8.2软件进行统计学分析。结果受试儿童总体FeNO水平中位数(四分位间距)为13.0 ppb(8.0～19.0 ppb),其中男童13.0ppb(10.0～19.5 ppb),女童为13.5 ppb(10.0～17.0 ppb),不同性别比较差异无统计学意义(P>0.05);FeNO与肺功能各参数[用力肺活量(FVC)、第1秒用力呼气量(FEV1)、FEV1/FVC、呼气峰流速(PEF)]亦无相关性(R2=0.016 0、0.013 9、0.014 4、0.007 5);FeNO水平与身高、年龄、体质量、BMI均无相关性(R2=0.062 3、0.044 0、0.098 3、0.037 2)。结论健康儿童FeNO中位数为13.0ppb[8.0～19.0 ppb],FeNO与性别、年龄、身高、体质量、BMI无相关性,与肺功能各参数之间亦无相关性,但二者密不可分,是全面评价儿童哮喘的呼吸道炎症的无创方法。     

哮喘患儿呼出气一氧化氮水平与肺功能相关性研究

目的 探讨处于稳定期哮喘患儿呼出气一氧化氮水平(FeNO)与肺功能中第一秒用力呼气容积(FEVl)的相关性.方法 选取2009年2月至2009年7月于中国医科大学附属盛京医院小儿哮喘门诊就诊的5～14岁的稳定期哮喘患儿53例,根据其是否应用吸入糖皮质激素规范化治疗分为激素治疗组和非激素治疗组,分别测定其FeNO水平和肺功能,分析FeNO水平和肺功能在两组患儿之间是否存在统计学差异,并比较两组患儿FeNO水平和肺功能指标是否存在相关性.结果 非激素治疗组患儿FeNO水平明显高于激素治疗组,且差异有显著性(P=0.005).激素治疗组患儿FEV1平均值为(95.152±8.993)%,非激素治疗组患儿FEVl平均值为(91.350±11.690)%,两组差异无显著性(P=0.932).非激素治疗组患儿FeNO水平与FEV1呈显著负相关性(r=-0.465,P=0.039).激素治疗组哮喘患儿FcNO水平与FEV1参数不相关(r=0.058,P=0.747).结论 处于稳定期的哮喘患儿,未应用吸入糖皮质激素规范化治疗时,其FeNO水平明显高于已用激素规范治疗患儿,测定FeNO水平可以作为一项很好的指标来评价哮喘患儿的气道炎症.     

Toll样受体2和4在金黄色葡萄球菌α-毒素诱导人单核-巨噬细胞凋亡过程中的作用

目的研究金黄色葡萄球菌的α-毒素阳性菌株Wood46、RN6390和金黄色葡萄球菌主要毒力因子α-毒素感染人外周血单核细胞后Toll样受体(TLRs)的表达及细胞凋亡情况。方法用Annexin V/磺化丙啶双染流式细胞仪检测人单核细胞凋亡;反转录-聚合酶链反应(RT-PCR)检测TLRs在信使核糖核酸(mRNA)的表达情况。结果金黄色葡萄球菌α-毒素阳性菌株Wood46、RN6390和α-毒素感染人外周血单核细胞后发生凋亡,TLR2和TLR4在Wood46和RN6390感染后的表达均明显增加(P<0.01),α-毒素感染人单核细胞后,TLR2和TLR4的表达呈时间依赖性升高。结论α-毒素可诱导人单核细胞凋亡,增加TLR2和TLR4的表达,在金黄色葡萄球菌的致病过程中起重要作用。     

先天性多发性支气管源性肺囊肿患儿1例

患儿女,6岁,以＂间断咳嗽10 d＂入院。近10 d轻咳,有少许黄色泡沫痰,无热,无呼吸困难,无胸痛。精神状态良好,活动后无气短,进食及睡眠好,二便正常。既往健康。本次住院前无呼吸系统疾病病史,无手术及外伤史。入院查体：体温36.5℃、脉搏86次/min、呼吸24次/min、血压85/50 mmHg。咽部略赤,扁桃体无肿大。呼吸平稳,胸廓对称,     

经支气管镜检查确诊支气管内膜结核合并肺炎支原体感染一例

患儿,女,9岁,以"间断发热伴咳嗽咯痰10 d"为主诉入院.患儿10d前无明显诱因出现发热,每7～8小时发热1次,热峰40℃,伴有寒战,手脚发凉.伴咳嗽,为阵咳,有痰,为黄白色痰.于当地医院静脉滴注红霉素、二代头孢、地塞米松治疗5d,发热及咳嗽无明显缓解.改为静脉滴注三代头孢、甲泼尼龙2d,热退1d,咳嗽咯痰无明显好转.1d前再次发热,体温38.0℃.偶有乏力,无午后低热、盗汗及消瘦.否认结核接触史.入院查体:T 36.3℃,P 88次/min,R 20次/min,BP 100/70 mm Hg(1mm Hg =0.133 kP),体重38 kg,神清状可,周身未见出血点及皮疹,浅表淋巴结未扪及肿大,咽赤,双扁桃体无肿大,胸廓平坦、对称,左肺听诊呼吸音稍弱,未闻及干湿性哕音,心音有力,心律齐,各瓣膜听诊区未闻及杂音,腹平软,全腹无压痛、反跳痛及肌紧张,肝脾肋下未触及,神经系统查体未见异常.辅助检查:肺炎支原体抗体-IgM阳性;肺炎支原体抗体(凝集法):1:1 280;结核抗体测定(胶体金法):弱阳性;肺炎衣原体抗体-IgM阳性;血常规:WBC 6.3×109/L;N 80.7％;RBC3.7×1012/L;Hb 129 g/L;PLT 234×109/L;CRP 33.00 mg/L;肝功能:白蛋白29.30 g/L,ALT 75 U/L;肺CT:左肺炎症,左肺上叶肺组织大部分实变(见图1).入院诊断:(1)左肺上叶大叶性肺炎;(2)肺炎支原体感染;(3)肺炎衣原体感染;(4)低蛋白血症;(5)肝功能受累;(6)结核感染待除外.入院后给予阿奇霉素联合头孢二代抗感染,患儿仍有持续发热,间隔3～4h1次,热峰39.5℃,伴咳嗽,有痰.     

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目的 研究高渗盐水激发试验及运动激发试验在哮喘儿童的临床应用,旨在寻求更适合哮喘儿童的气道反应性检测的方法方法收集中国医科大学附属盛京医院2007年5月至2008年6月符合儿童支气管哮喘防治常规诊断标准的哮喘缓解期患儿34例,年龄5～13岁,在规定时间内先后做气道高渗盐水激发试验和运动激发试验.结果 同一哮喘患儿高渗盐水激发试验的敏感性显著高于运动激发试验(P<0.01).结论 高渗盐水激发试验的敏感性和特异性高于运动激发试验,而且设备低廉,方法简单、易配合,安全,副反应少,尤其适用于在哮喘治疗期间动态观察儿童气道的反应性,对指导药物治疗有重要价值.