大鼠烫伤后肺泡表面活性物质系统的变化

本研究应用电镜组化和生化分析方法,对大鼠40%体表面积全层皮肤烫伤后肺泡表面活性物质系统改变进行了48小时动态观察。结果发现烫伤后6小时即可见表面活性物质层失连续、聚集和脱落,肺泡Ⅱ型上皮细胞胞浆和板层体空泡化,部分Ⅱ型上皮细胞坏死,肺间质中性白细胞浸润,表面活性物质提取物中双饱和卵磷脂减少,随后发现局灶性肺泡萎陷,提示肺泡表面活性物质系统损伤在烧伤后ARDS的发生、发展中可能具有重要意义。     

肺表面活性物质对大鼠肺损伤后氧合功能的影响

目的和方法：本研究利用氧自由基所致的大鼠肺损伤模型,对肺损伤后肺表面活性物质（ＰＳ）病理改变和外源性ＰＳ替代治疗的作用进行了探讨。结果：大鼠气道滴入黄嘌呤和黄嘌呤氧化酶２４ｈ后,ＰａＯ２和胸肺顺应性显著下降;肺系数明显增高,组织学观察可见炎症性肺水肿。肺支气管灌洗液分析结果表明ＰＳ含量减少,蛋白含量增高。应用外源性ＰＳ治疗后,ＰａＯ２从处理前３２４±８６ｋＰａ上升到４７５±２９ｋＰａ（Ｐ＜００１）。结论：（１）肺损伤后的不同阶段ＰＳ的病理变化可能是不一致的;（２）外源性ＰＳ的替代治疗有明显效果。     

部分液体通气对内毒素肺损伤肺表面活性物质系统超微结构的影响

目的:研究部分液体通气对内毒素肺损伤大鼠肺表面活性物质(pulmonarysurfactant,PS)系统超微结构的影响。方法:运用电子显微镜细胞化学方法,对内毒素肺损伤鼠PS系统进行观察及部分液体通气对其的影响。结果:内毒素肺损伤后可见PS层失去连续性,呈断裂或堆积;肺泡II型细胞内板层小体、线粒体空泡化,少数发生坏死并崩解、脱落进入肺泡腔。液体通气+肺损伤组PS系统损伤程度明显低于内毒素肺损伤组。结论:液体通气可明显改善内毒素肺损伤时PS系统的损伤。     

金黄地鼠实验性肺气肿肺泡Ⅱ型上皮表面活性物质蛋白A和B的 …

目的 观察金黄地鼠实验性肺气肿肺泡Ⅱ型上皮表面活性物质蛋白（ＳＰ）Ａ和Ｂ的变化。方法 金黄地鼠气管注入弹性蛋白酶后,分别于注入弹性蛋白酶的３０、６０和９０ｄ处死,肺组织经光镜检查和图像分析后,再行ＳＰ－Ａ和ＳＰ－Ｂ免疫组化染色和形态定量;同时进行透射电镜观察。结果 注入弹性蛋白酶后第３０、６０和９０ｄ肺平均内衬间隔明显增大（Ｐ〈０．０１）;免疫组化显示注入弹性蛋白酶后３０ｄ肺泡Ⅱ型上皮细胞ＳＰ－Ａ     

人肺表面活性物质结合蛋白B的研究现状

人肺表面活性物质结合蛋白Ｂ（ＳＰ－Ｂ）为肺泡表面活性物质中的重要成份。具有生物活性的ＳＰ－Ｂ存在于肺泡Ⅱ上皮细胞、肺泡巨噬细胞和肺泡中，在体外ＳＰ－Ｂ与磷脂的复合物即具有肺表面活性物质的大部分生物活性，而在体内可增强肺的顺应性，人ＳＰ－Ｂ基因定位第２号染色体，其基因表达受多种因素调节。遗传性ＳＰ－Ｂ缺乏病例已见报道。     

ARDS时肺表面活性物质系统的变化研究进展

肺表面活性物质系统是维持正常呼吸功能的基础，其总量、组分、代谢及活性的改变是成人呼吸窘迫综合征发病机制中的重要环节之一。     

内毒素对大鼠肺泡Ⅱ型上皮细胞的损伤作用

目的：研究急性肺损伤时内毒素主要成分脂多糖（LPS）对肺泡Ⅱ型上皮细胞（AT-Ⅱ）的损伤作用。方法：18只SD大鼠随机分为生理盐水对照组、LPS模型组。通过颈外静脉给药4h后处死动物,收集肺泡灌洗液（BALF）测定表面张力、总磷脂含量（TPL）、乳酸脱氢酶（LDH）、碱性磷酸酶（AKP）、丙二醛（MDA）及总蛋白（TP）含量;取右肺下叶,行HE染色光镜观察。结果：与对照组相比,LPS可增加表面张力[（23．12±2．8）vs（19．6±2．5）mN·m^-1,P〈0．05],并提高BALF中LDH活性[（8．2±1．9）vs（4．7±1．9）μkat·L^-1,P〈0．05]以及AKP活性[（256±101）vs（102±81）nkat·L^-1,P〈0．01];增加TP含量[（85±31）vs（29±16）g·L^-1,P〈0．01]和MDA含量;降低BALF中TPL含量[（370±57）vs（432±43）μg·kg^-1,P〈0．05]。同时光镜下发现LPS组呈典型间质性肺水肿表现。结论：LPS可以引起AT-Ⅱ的损伤,并抑制其合成、分泌肺表面活性物质。     

肺泡外肺表面活性物质结合蛋白A研究进展

肺表面活性物质结合蛋白A(SP A)是肺表面活性物质中最主要的蛋白成分 ,主要由Ⅱ型肺泡上皮细胞及clara细胞分泌。研究发现 ,在肺泡外也存在相对低水平的SP A ,在传导气道、中耳、咽鼓管、鼻旁窦、胃肠道、生殖道、胸腺、脾脏、间皮及滑膜细胞内均可检测到SP AmRNA及蛋白 ,SP A可与病原及巨噬细胞结合 ,增强巨噬细胞吞噬杀灭病原 ,这些部位的SP A可能与宿主防御有关 ,在某些部位也有降低表面张力的作用     

大鼠复合内毒素血症致肺微循环变化与肺泡表面活性物质功能的关系

本实验应用大鼠烫伤复合内毒素血症的模型,制备肺组织超薄切片,进行透射电镜观察,同时测定其肺泡表面活性物质的功能;结合白细胞计数、血清和肺组织内二醛(MDA)含量以及超氧化物歧化酶(SOD)活性的测定。结果显示,肺毛细血管内粒细胞增多并粘附于内皮细胞膜;内皮细胞受损。肺泡表面活性物质功能明显降低。血清和肺组织MDA含量明显增加,SOD活性则显著下降。用SOD治疗能明显改善上述病变。本实验结果提示,肺微循环障碍是烫伤复合内毒素血症致急性肺损伤时肺泡表面活性物质功能下降的病理基础,与白细胞在肺血管内陷落、激活、释放自由基有关。SOD对此有一定的保护作用。     

大鼠烫伤复合内毒素血症时肺微循环与肺泡表面活性物质功能的变化

本实验应用大鼠烫伤复合内毒素血症的模型,制备肺组织超薄切片,进行透射电镜观察,同时测定其肺泡表面活性物质的功能;并做白细胞计数、血清和肺组织丙二醛含量以及超氧化物歧化酶活性的测定。结果显示,肺毛细血管内粒细胞增多并粘附于内皮细胞膜;内皮细胞胞浆空泡化,胞膜缺损、断裂;内皮细胞下、肺     

Nonionic surfactant attenuates acute lung injury by restoring epithelial integrity and alveolar fluid clearance

Introduction: Acute lung injury (ALI) has a great impact and a high mortality rate in intensive care units (ICUs). Excessive air may enter the lungs, causing pulmonary air embolism (AE)-induced ALI. Some invasive iatrogenic procedures cause pulmonary AE-induced ALI, with the presentation of severe inflammatory reactions, hypoxia, and pulmonary hypertension. Pulmonary surfactants are vital in the lungs to reduce the surface tension and inflammation. Nonionic surfactants (NIS) are a kind of surfactants without electric charge on their hydrophilic parts. Studies on NIS in AE-induced ALI are limited. We aimed to study the protective effects and mechanisms of NIS in AE-induced ALI.Materials and methods: Five different groups (n = 6 in each group) were created: sham, AE, AE + NIS pretreatment (0.5 mg/kg), AE + NIS pretreatment (1 mg/kg), and AE + post-AE NIS (1 mg/kg). AE-induced ALI was introduced by the infusion of air via the pulmonary artery. Aerosolized NIS were administered via tracheostomy.Results: Pulmonary AE-induced ALI showed destruction of the alveolar cell integrity with increased pulmonary microvascular permeability, pulmonary vascular resistance, pulmonary edema, and lung inflammation. The activation of nuclear factor-κB (NF-κB) increased the expression of pro-inflammatory cytokines, and sodium-potassium-chloride co-transporter isoform 1 (NKCC1). The pretreatment with NIS (1 mg/kg) prominently maintained the integrity of the epithelial lining and suppressed the expression of NF-κB, pro-inflammatory cytokines, and NKCC1, subsequently reducing AE-induced ALI.Conclusions: NIS maintained the integrity of the epithelial lining and suppressed the expression of NF-κB, pro-inflammatory cytokines, and NKCC1, thereby reducing hyperpermeability, pulmonary edema, and inflammation in ALI.     

Structural changes in the lungs and phospholipids of the lung surfactant in rats with experimental bleomycin pneumosclerosis

Central Roentgeno-Radiological Research Institute, Ministry of Health of the USSR. Institute of Pulmonology, Ministry of Health of the USSR, Leningrad. I. M. Sechenov Moscow Medical Academy. (Presented by Academician of the Academy of Medical Sciences of the USSR A. N. Klimov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 11, pp. 534–536, November, 1991.     

急性肺损伤大鼠肺组织β和β2受体及β2受体mRNA表达的变化

目的：观察急性肺损伤（ＡＬＩ）大鼠肺组织β、β２受体和β２受体ｍＲＮＡ含量的变化,探讨上述变化与ＡＬＩ的关系及β２受体变化可能的分子机制。方法：静注内毒素复制大鼠ＡＬＩ模型,肺组织β、β２受体及β２受体ｍＲＮＡ含量,分别用放射性配基结合分析法和斑点杂交技术测定。结果：静注内毒素后１、４、６ｈ,大鼠肺组织β和β２受体的最大结合容量（Ｂｍａｘ）均明显低于正常对照组（Ｐ＜０．０１）,尤以β２受体为甚;静注内毒素后４及６小时,大鼠肺组织β２受体ｍＲＮＡ含量分别下降至正常对照组的７６４％±１９６％（Ｐ＜０．０１）和５２８％±２０４％（Ｐ＜０．０１）。结论：肺组织β受体数目的减少在ＡＬＩ发生发展中可能起一定的作用,β２受体数目的减少可能与ＡＬＩ关系更密切;β２受体ｍＲＮＡ含量的减少可能是ＡＬＩ后一定阶段肺组织β２受体数目减少的原因之一。     

急性缺氧小鼠脑组织磷脂组分的变化

本工作观察并比较了１次缺氧，重复４次缺氧以及未经缺氧的正常小鼠脑细胞中磷脂组分含量的变化。结果表明，１次缺氧鼠磷脂酰乙醇胺（ｐｈｏｓｐｈａｔｉｄｙｌ ｅｔｈａｎｏｌａｍｉｎｅｓ，ＰＥ）。磷脂酰丝氨酸（ｐｈｏｓｐｈａｔｉｄｙｌ ｓｅｒｉｎｅ，ＰＳ）、含量显著升高，磷脂酰胆碱（ｐｈｏｓｐｈａｔｉｄｙｌ ｃｈｏｌｉｎｅｓ，ＰＣ）、鞘磷脂（ｓｐｈｉｎｇｏｍｙｅｌｉｎｓ，ＳＭ）含量显著下降；但经４次重复缺氧     

The surfactant system of the adult lung: physiology and clinical perspectives

Summary Pulmonary surfactant is synthesized and secreted by alveolar type II cells and constitutes an important component of the alveolar lining fluid. It comprises a unique mixture of phospholipids and surfactant-specific proteins. More than 30 years after its first biochemical characterization, knowledge of the composition and functions of the surfactant complex has grown considerably. Its classically known role is to decrease surface tension in alveolar air spaces to a degree that facilitates adequate ventilation of the peripheral lung. More recently, other important surfactant functions have come into view. Probably most notable among these, surfactant has been demonstrated to enhance local pulmonary defense mechanisms and to modulate immune responses in the alveolar milieu. These findings have prompted interest in the role and the possible alterations of the surfactant system in a variety of lung diseases and in environmental impacts on the lung. However, only a limited number of studies investigating surfactant changes in human lung disease have hitherto been published. Preliminary results suggest that surfactant analyses, e.g., from bronchoalveolar lavage fluids, may reveal quantitative and qualitative abnormalities of the surfactant system in human lung disorders. It is hypothesized that in the future, surfactant studies may become one of our clinical tools to evaluate the activity and severity of peripheral lung diseases. In certain disorders they may also gain diagnostic significance. Further clinical studies will be necessary to investigate the potential therapeutic benefits of surfactant substitution and the usefulness of pharmacologic manipulation of the secretory activity of alveolar type II cells in pulmonary medicine.Abbreviations PC phospatidyleholine - DPPC dipalmitoylphosphatidylcholine - PG phosphatidylglycerol - PI phosphatidylinositol - SP-A, SP-B SP-C, SP-D surfactant-specific proteins A, B, C, and D - ARDS adult respiratory distress syndrome - IRDS infant respiratory distress syndrome - BAL bronchoalveolar lavage - IPF idiopathic pulmonary fibrosis - HP hypersensitivity pneumonitis - DIPD drug-induced pulmonary disease