人肺毛细血管和肺泡铸型的扫描电镜观察

本文用扫描电镜观察了ABS丁酮溶液灌注人肺泡及其毛细血管的结构,结果如下: 1.自胸膜下和小叶间隔面观察了肺泡的铸型。人肺泡是不规则的多面体形,大小不等,表面光滑,有较多的Ⅱ型细胞压迹。两肺泡之间的桥样结构为肺泡孔、数量、大小均不等。 2.胸膜下和小叶间隔的肺泡毛细血管相互移行,形态和疏密度一致。毛细血管网都稀疏,但比犬肺胸膜下的毛细血管网密集。 3.肺泡隔内的毛细血管为单层,而且密集,毛细血管本身的直径比网孔径要大。该部毛细血管主要由胸膜下或小叶间隔的毛细血管延续而来。     

大鼠肺微血管和肺泡铸型的扫描电镜观察

用扫描电镜观察以甲基丙烯酸甲酯灌注鼠的肺微血管和肺泡。胸膜下毛细血管较稀疏,网孔粗大。毛细血管部分成锐角折返,亦可见毛细血管盲端。肺泡隔毛细血管均成扁平状膨大,且相互吻合成单层密集网。肺泡铸型为大小不等、不规则的多面体,表面可见肺泡Ⅱ型细胞核之压迹。两肺泡之间可见呈桥式连接的肺泡孔,亦可见部分呈三通管样相连。     

人肺毛细血管和肺泡铸型的扫描电镜观察(文摘)

本文用扫描电镜观察了 ABS 丁酮溶液灌注人肺泡及其毛细血管的结构,其结果如下:自胸膜和小叶间隔面观察了肺泡的铸型。人肺泡呈不规则的多面体形,大小不等,表面光滑,有较多的Ⅱ型细胞顶端压迹。两肺泡之间的桥样结构为肺泡孔,其数量、大小均不等。并讨论了肺泡孔的机能。胸膜下和小叶间隔的肺泡毛细血管相     

肾小球微血管构型的扫描电子显微镜观察

应用微血管铸型扫描电镜技术研究8例成人肾脏的肾小球微血管构筑,结果发现:1.输入小动脉在肾小球血管极处分为2～5支小球内小叶微动脉。输入小动脉血管铸型的直径为126.35±20.5μm。2.肾小球是由小球内小叶微动脉、毛细血管、毛细血管网小叶间交通支和毛细血管输出根所构成的近似于球状体,小球内每个毛细血管网小叶均是一个独立的机能解剖学单位;3.299个肾小球均有一支输出小动脉,只有一个肾小球有两支输出小动脉。输出小动脉的血管铸型直径为91.35±11.7μm。4.输出小动脉起始处具有毛细血管前括约肌装置,此结构在调控肾小球内的微循环血流有着重要意义。     

急性肺栓塞的确定诊断

1　同位素扫描肺同位素扫描属无创性检查 ,且可反复检查 ,是筛选本病实用的检查方法。分肺灌注显像和肺通气显像。肺灌注显像是用标记的放射性核素99ｍＴｃ静脉注射 ,以达到肺毛细血管的密度来评价肺血流分布的方法。原理 :肺泡毛细血管的直径 7～ 9μｍ ,当静脉内注射大于其直径的某种放射性核素标记的微粒 ,如99ｍＴｃ标记的大颗粒聚合人血清白蛋白 (99ｍＴｃ ＭＡＡ)微粒的直径在 1 0～ 90 μｍ ,它们随血流到达微小动脉 ,可一过性的嵌顿在肺毛细血管或肺小动脉内 ,局部微栓塞的放射性微粒数与该处的肺血流灌注量成正比。因此 ,当体外用…     

缺氧性肺动脉高压和肺源性心脏病的防治

肺血液循环概述 肺的血液循环由肺循环和支气管循环两部分组成,主要功能是收集全身的静脉血液,靠右心室泵的作用,使其通过肺泡毛细血管进行气体交换,然后再将动脉化的血液运送至左心房和左心室而输送到全身。肺循环血管与体循环相比,肺血管短粗且壁薄,肺微动脉壁的平滑肌稀少,但仍有神经支配,肺毛细血管由结缔组织支架撑开形成围绕肺泡囊的密集网络。据估计,在静息状态下肺毛细血管的表面积达60-70平方米,约为体表面积的40倍,运动期间可增至90平方米,这是由于肺内以前闭合的血管全部开放所致。主肺动脉平均压为15mmHg,收缩压为25mmHg,舒张压为8mmHg,故呈搏动性。由于不可能直接测量毛细血管的压力,所以肺毛细血管压无准确数值,估计应低于肺小动脉而高     

肺容积和肺泡表面张力对肺血管阻力的影响

灌流狗在体左下肺叶,在肺内压力-容积环上分别选择等压和等容两点,比较吸气和呼气支上相等肺泡压或相等肺容积时的肺血管阻力。呼吸周期中肺动脉压的改变主要取决于肺泡血管阻力的变化。呼气期由肺泡表面液体层产生的向肺泡中心的表面张力较吸气期低,使肺泡压能更有效地传递至肺泡血管.估计在中等肺容积时,呼气期较吸气期毛细血管周围压高465～505Pa(3.5～3.8mmHg).     

胎儿肾小球血管构筑

应用微血管铸型扫描电镜观察１５例２０～３８周胎儿肾小球血管构筑。发现，球型肾小球占多数（７１．５％），菊花型（１６％）和混合型（１２．５％）较少，肾小球的类型是由胚胎早期发育所决定。入球与出球小动脉多为１支，少数有２支以上，在入、出球小动脉之间未观察到有直接吻合的血管，但少数肾小球与肾小球之间有毛细血管相交通，或肾小球与肾小球之间接触部分毛细血管形成直接吻合。此外，还观察到较少的近足月龄胎儿肾小球旁器内毛细血管的构筑，其毛细血管分布较局限，毛细血管直径大于其形成网眼的直径。     

肝硬化合并肺血管病变：附30例病理解剖分析

随机复查尸检30例肝硬化HE染色肺切片。观察肺泡水平即500μm以下肺小动静脉、毛细血管的分布及变性状态,并将其它病尸检10例作对照。30例中三尖瓣剖开口径扩张>12cm者20%;左右肺重均>对照组;肺淤血100%;肺小动脉变性16.6%,500μm以下肺小动脉数目100倍视野显现增多者73%;扩张肥厚且数目增加、中膜平滑肌增厚者33%(壁厚平均22.57μm);镜下肺胸膜20%局部血管扩张与食道静脉曲张图象相似。如作肺胸膜活检,发现500μm以下肺小动脉及毛细血管有上述所见者有助于肺动脉高压诊断。     

舌肌和翼内肌微血管几何学构筑的研究

本文应用微血管腐蚀铸型扫描电镜,观察了2例3岁幼儿的舌肌和翼内肌的微血管构型。在扫描电镜下,舌肌内的毛细血管网构型分三类:1.花蕊样毛细血管袢;2.云朵样毛细血管网;3.多角形套状毛细血管网。毛细血管铸型的直径为5.3±1.5μm,描述了动脉铸型表面上的内皮细胞核压痕和前毛细血管括约肌压痕的形态特征。讨论了血管袢的结构形态及其机能意义,为理解骨骼肌的微循环的过程提供了形态学基础。     

肾小球的扫描电子显微镜观察

我们对6只狗的左、右肾进行了扫描电镜观察,结果表明肾小球的外部构筑,可分为球型、菊花型和混合型。在有的肾小球的入球小动脉和出球小动脉之间,或邻近的两出球小动脉之间,有长短不一、粗细不等的血管吻合支存在。在肾小球的血管极处,即肾小球旁器所在部,非血管成分被腐蚀,但清楚地显示出肾小球旁器内毛细血管网的立体构型,表现为管径粗、网孔小、网眼密和血管分布近似三角形。这种构型特点,与该部位血流速率快、流量大有密切关系。     

THE EFFECT OF OXYGEN INTOXICATION ON THE MORPHO- LOGY OF INTERCELLULAR FUNCTIONS OF PULMONARY ENDOTHELIUM AND ALVEOLAR EPITHELIUM A FREEZE-FRACTURE STUDY

Intercellular junctions in the alveolar epithelium and in the capillary endothelium in the lungs of 4 sheep with oxygen intoxication and 3 control sheep are studied by freeze-fracture. Under electron microscope,it was found that there was no significant difference between the number of strands, both in the epithelium and in the endothelium, in the oxygen intoxication group and the control group. However, the incidences of discontinuity, irregularity and free- ended strands were higher in the oxygen intoxicated group than in the control. The differences of most of these features were highly significant (p<0.005). In addition, in the oxygen intoxicated group some epithelial junctions showed that the meshes of the network were extended significantly. These phenom ena may indicate destruction or degeneration of the junctional elements and may partly explain the route of fluid leakage and the occurrence of pul- monary edema induced by breathing pure oxygen.     

百草枯所致大鼠弥漫性肺损伤的病理特点

作者选用ＳＤ大鼠进行腹腔内一次性注入百草枯２５ｍｇ／ｋｇ后，在７个不同时间点观察其肺病理组织和超微结构改变。结果显示：百草枯可引起弥漫性毛细血管内皮细胞和肺泡１型上皮细胞为主的整层气一血屏障结构的损害，主要表现为肺泡水肿、出血、透明膜形成和（或）程度不等的肺泡炎，当损伤不能完全修复时则局部终结为纤维化。     

小儿内脏器官的形态学研究(七)——新生儿气管和肺的组织学观察

新生儿呼吸器官—气管和肺的结构已基本发育完全。气管上皮为假复层纤毛柱状上皮。软骨内同源群细胞很少见。肺泡上皮以立方形细胞较多。肺泡隔较厚,毛细血管丰富。     

SARS尸检的肺部病理改变

目的 通过研究严重急性呼吸综合征(severe acute respiratory syndrome,SAPS)患者的尸检肺部标本。总结SAPS的肺部病变特点及发病机制。方法 详细检查SARS患者肺脏标本的大体特点,并用常规方法研究显微光镜下SAPS累及各肺叶的病变特点。结果 7例SAPS患者的双肺均明显膨胀,镜下表现以弥漫性肺泡损伤(DAD)不同时期的病变为主。7例均有肺水肿及透明膜形成,肺水肿尤以早期明显。病程超过3周者开始有肺泡内机化及肺间质纤维化,造成肺泡的纤维性闭塞。几乎每例都可见到小血管内的微血栓和肺出血、散在的小叶性肺炎、肺泡上皮脱落、增生等病变。2例可见曲霉菌感染,l例累及左全肺及右肺部分区域,l例出现在肺门淋巴结。肺门淋巴结多表现为充血、出血及淋巴组织减少,窦组织细胞增多。结论 SAPS肺可能为SAPS病毒造成的弥漫性肺泡损伤,表现为肺泡上皮及毛细血管的严重损伤导致肺水肿和肺泡及细支气管的纤维索性渗出性炎症,出现透明膜。继而出现肺泡内机化及肺泡间隔的成纤维细胞增生,共同使肺泡萎陷、机化,最终形成纤维化实变。肺门淋巴组织的减少可能是此病影响免疫系统的又一形态学表现。     

阿霉素白蛋白磁纳米粒在正常肝脏的靶向性

目的：观察阿霉素白蛋白磁纳米粒在正常肝脏中的磁靶向性。并观察阿霉素白蛋白磁纳米粒在全身各脏器的分布特征。方法：大鼠正中开腹,胃十二指肠动脉插管固定。实验组,左肝外叶加磁场,肝动脉注射阿霉素白蛋白的磁纳米粒（相当于阿霉素0．5mg/kg),磁场应用30min移去磁场后,动物立即处死,对照组：左肝外叶外不加磁场,肝动脉注射同等剂量的纳米粒后30min处死。动物处死后,立即取靶区肝、非靶区肝、心、肾、脾、肺、小肠和胃作γ计数。肝组织作组织学切片。结果：左肝外叶应用磁场30min后,磁共肝组织的放射活性较非磁共肝组织的放射活性明显增加（P＜0．0001）,磁区肝组织与非磁区肝组织的放射活性比值为2．6。而对照组磁区肝组织与非磁区肝组织的放射活性之间无统计学差异。肝外脏器的放射活性明显降低。除实验组肺的放射活性较对照组明显下降外,其它脏器两组之间没有统计学差异,另外,实验组,心、肾、脾、肺和小肠与靶区肝组织和的放射活性比值较对照组明显降低,胃与靶区肝组织的放射活性比值两组之间无统计学差异。注入纳米粒的70％－80％分布于肝脏,其它脏器含量极少。病理切片显示磁共小动脉中见大量纳米粒存在,对照组及非磁共肝中纳米粒很少见。结论：阿霉素白蛋白磁纳米粒在正常肝脏组织中有明显的磁靶向性,阿霉素白蛋白磁纳米粒主要分布于肝脏,其它脏器含量较少。实验组心、肾、脾、肺和小肠与靶区组织的放射活性比值明显降低,说明磁的存在使这些脏器的相对药物暴露明显减少。     

Alveolar stability under different combinations of positive end-expiratory pressure and tidal volume: alveolar microscopy in isolated injured rat lungs

Background High positive end-expiratory pressure （PEEP） and low tidal volume （VT） ventilation is thought to be a protective ventilation strategy. It is hypothesized that the stabilization of collapsible alveoli during expiration contributes to lung protection. However, this hypothesis came from analysis of indirect indices like the analysis of the pressure-volume curve of the lung. The purpose of this study was to investigate isolated healthy and injured rat lungs by means of alveolar microscopy, in which combination of PEEP and VT is beneficial with respect to alveolar stability （I-E%）. Methods Alveolar stability was investigated in isolated, non-perfused mechanically ventilated rat lungs. Injured lungs were compared with normal lungs. For both groups three PEEP settings （5, 10, 20 cmH20） were combined with three VT settings （6, 10, 15 ml/kg） resulting in nine PEEP-VT combinations per group. Analysis was performed by alveolar microscopy. Results In normal lungs alveolar stability persisted in all PEEP-VT combinations （I-E% （3.2±11.0）%）. There was no significant difference using different settings （P 〉0.01）. In contrast, alveoli in injured lungs were extremely instable at PEEP levels of 5 cmH20 （mean I-E% 100%） and 10 cmH2O （mean I-E% （30.7±16.8）%）; only at a PEEP of 20 cmH20 were alveoli stabilized （mean I-E% of （0.2±9.3）%）. Conclusions In isolated healthy lungs alveolar stability is almost unaffected by different settings of PEEP and VT. In isolated injured lungs only a high PEEP level of 20 cmH2O resulted in stabilized alveoli whereas lower PEEP levels are associated with alveolar instability.     

Protective effect of rhubarb on endotoxin-induced acute lung injury.

To approach the mechanism of lipopolysaccharide (LPS) in causing acute lung injury (ALI) and the protective effect of rhubarb and dexamethasone, lung specimens were examined with macroscopy, microscopy, electron microscopy and the biological markers of ALI including lung wet/dry weight, the rate of neutrophils and protein content in the pulmonary alveolar lavage fluid, pulmonary capillary permeability and pulmonary alveolar permeability index were observed. The mechanism of the ALI is mainly due to direct injury of alveolar epithelium and pulmonary vascular endothelium. Rhubarb and dexamethasone could significantly reduce the edema of the lung tissue, decrease the red blood cell exudation, neutrophil infiltration and plasma protein exudation in the alveoli and all the biological markers in comparison with the ALI model rats, indicating they have protective action on vascular endothelium and alveolar epithelium.     

Pathological study on severe acute respiratory syndrome

Objective To study the pathological characteristics of severe acute respiratory syndrome (SARS)and its relationship to clinical manifestation.Methods Tissue specimens from 3 autopsies of probable SARS cases were studied by microscope,and the clinical data was reviewed.Results The typical pathological changes of lungs were diffuse hemorrhaging on the surface. A combination of serous, fibrinous and hemorrhagic inflammation was seen in most of the pulmonary alveoli with the engorgement of capillaries and detection of micro-thrombosis in some of these capillaries. Pulmonary alveoli thickened with interstitial mononuclear inflammatory infiltrates, suffered diffuse alveolar damage, experienced desquamation of pneumocytes and had hyaline-membrane formation, fibrinoid materials, and erythrocytes in alveolar spaces. There were thromboembolisms in some bronchial arteries. Furthermore, hemorrhagic necrosis was also evident in lymph nodes and spleen with the attenuation of lymphocytes. Other atypical pathological changes, such as hydropic degeneration, fatty degeneration, interstitial cell proliferation and lesions having existed before hospitalization were observed in the liver, heart, kidney and pancreas.Conclusion Severe damage to the pulmonary and immunological systems is responsible for the clinical features of SARS and may lead to the death of patients.