肺泡毛细血管

4）肺泡毛细血管床内表面积（Sc）：3525.05±569.91cm~2/左右肺；

4 ) the internal surface area of the alveolar capillary bed ( S_C ) was 3525.05 ± 569.91cm ~ 2 ;

3）肺泡毛细血管床容积（Vc）0.42+O.09cm~3/左右肺；

3 ) the volume of alveolar capillary bed ( V_C ) was 0.42 ± 0.09 cm ~ 3 / both lungs ;

结论中度低温对ALI大鼠可通过减轻肺内PMN聚集，降低肺泡毛细血管膜通透性，在一定程度上减轻了肺损伤。

Conclusion Moderate hypothermia significantly decreases the increased permeability of alveolar capillary membrane in a rat model of ALI induced by LPS .

目的研究特发性间质性肺炎（IIP）患者肺泡毛细血管膜弥散能力（DM）和肺泡毛细血管床容量（VC）变化及特点。

Objective To investigate diffusion capacity of pulmonary capillary membrane and pulmonary capillary volume in patients with idiopathic interstitial pneumonia ( IIP ) .

结果：N株感染后期，肝血窦、肾间质和毛细血管、肺泡毛细血管含有较多的感染疟原虫红细胞，肺泡壁毛细血管内皮细胞有较多的突起与疟原虫感染红细胞相接触。

Results : Congestion and more parasite infected red blood cells in hepatic sinusoids , renal interstitium , capillaries of the liver , kidney and lungs in late period of the infection with the N strain were observed .

结果：RSV肺炎病理改变严重，肺泡毛细血管出现淤血、微血栓。

Results : Pathological changes in mice with RSV pneumonia were serious with extravasation of blood and embolism in alveolar capillary .

目的探讨中度低温对脂多糖（LPS）诱导急性肺损伤（ALI）大鼠肺泡毛细血管膜通透性的影响。

Objective To investigate the effects of moderate hypothermia on the permeability of alveolar capillary membrane in acute lung injury ( ALI ) induced by lipopolysaccharide ( LPS ) .

结论：BALF中SP-A的含量降低可以早期准确地反映肺泡毛细血管膜的损伤程度；

Conclusion : The decrease of SP-A in BALF could indicate accurately the injury of alveoli capillary membrane in the early stage .

结论：①正常C57BL/6小鼠肺泡毛细血管内皮细胞以TM表达为主型，而非vWf表达为主型。

CONCLUSION : These results suggest that TM dominant phenotype endothelial cells , rather than vWf dominant phenotype , are the major ones of alveolar capillaries in normal C57BL / 6 mice lungs .

肺泡毛细血管内血栓的发生率逐渐增高；染毒后90d出现了肺泡的萎缩和纤维化。

The capillary thrombosis became serious . After 90 days , the shrinks and fibrosis of alveolar occurred .

LVRS术后肺弥散功能、动脉血氧分压、低氧血症的显著改善，与肺毛细血管床容量的增加显著相关，与肺泡毛细血管膜弥散量的增加无明显关系。

The diffusing function , PaO2 and anoxia were significantly improved after LVRS closely relating to the increased Vc other than Dm .

有研究表明肺血管内皮细胞间完整性的破坏与血浆基质金属蛋白酶-9（MMP-9）的关系最为密切，MMP-9表达增多，活性升高，与肺组织损伤、肺泡毛细血管通透性升高密切相关。

Research indicated that the damage of pulmonary vascular endothelial cell and plasma matrix metalloproteinase - 9 ( MMP-9 ) are most closely related . The increase of MMP-9 expression and activity are closed related to lung tissue damage and alveolar capillary permeability increase .

作者认为ACST引发急性肺损伤与内毒素引起的氧自由基释放，从而引发肺泡毛细血管内皮细胞的脂质过氧化损害有关，而肺组织抗氧化物质的不足可能是促进肺损伤的因素之一。

These suggest that acute lung injury induced by ACST is referable to the lipid peroxidation damage to the lung blood capillaries which is due to increased LPO and decreased antioxidants including V. E.

结果：①正常C57BL/6小鼠肺泡毛细血管内皮细胞表面显示多数连续性线样TM荧光而vWf较少阳性，肺微小血管内皮细胞呈现vWf阳性。

RESULTS : ① The normal lungs showed multiple continuous linear positive staining of TM and seldom positive of vWf on the surface of endothelium of alveolar capillaries . Meanwhile , blood vessels exhibited considerable positive of vWf in endothelial cell in normal C57BL / 6 mice .

随着心功能的改善，术后6～12个月，患者的通气功能逐渐改善，但DLCO并不增加，推测可能与患者术后肺泡毛细血管容量减少以及肺组织结构损害不可逆性改变有关。

The pulmonary ventilative function was gradually improved with the improvement of heart function at 6 to 12 months after MVR . But the DLCO was not increased implying the decrease of pulmonary capillary blood volume after MVR and endurance of irreversible lung structural damage .

一种肺泡毛细血管发育不良伴十二指肠反常扩张的十二指肠闭锁的新合并症

A novel association of alveolar capillary dysplasia and duodenal atresia with paradoxical dilatation of the duodenum

特发性间质性肺炎患者肺泡毛细血管膜弥散能力和肺毛细血管床容量的研究

The investigation of pulmonary membrane diffusing capacity and pulmonary capillary blood volume in patients with idiopathic interstitial pneumonia

犬油酸型呼吸窘迫综合征时肺泡毛细血管通透性的变化及其早期诊断价值

Change of pulmonary microvascular permeability in dogs with respiratory distress syndrome induced by oleic acid : Role in diagnosis

结论：肺气肿肺弥散功能下降，与肺泡毛细血管膜弥散量、肺毛细血管床容量有关.硼膜中的含氢量测量

CONCLUSION : Dm and Vc may be involved in the impairment of the lung diffusing function . Measurement of Hydrogen Content in Boron Film

传统的理论认为：肺水肿的发病机制主要是由于液体静水压过高（心源性肺水肿）和肺泡毛细血管通透性增加（非心源性）所致。

In traditional theory , development of pulmonary edema mainly as a result of the increase in hydrostatic pressure ( cardiogenic edema ) and capillary permeability ( noncardiogenic edema ) .

由肺内炎症细胞（如嗜中性粒细胞、巨噬细胞）为主导的肺内炎症反应失控导致的肺泡毛细血管膜损伤是形成肺毛细血管通透性增高肺水肿的病理基础。

Inflammatory corpuscle in lung ( for example neutrophil 、 macrophagus ) lost of control could lead to damage of alveolar capillary membrane which is the base of pulmonary capillary vasopermeability increasing .

肺泡毛细血管网眼多呈椭圆形、三角形、多边形及不规则形，毛细血管直径7～11μm，网眼孔径8～25μm；

The pulmonary capillary mesh is elliptic , triangular , polygonal or irregular . The diameter of the alveolar capillary is 7 ~ 11 μ m. The diameter of the mesh is 8 ~ 25 μ m.

肺泡-毛细血管的损伤是ALI的发病基础，微血管内皮细胞作为血管内外物质交换的一道重要屏障，是循环血流剪切力和血中危险因素的主要靶目标，因而最容易并且最早受到伤害。

Pulmonary vascular endothelial cells , as the important barrier for material exchange in and out vascellum , are main target for blood current shearing force and risk factor in blood .

离子跨小鼠肺泡与毛细血管屏障转运的胸膜表面荧光方法

Pleural Surface Fluorescence Measurement of Ion Transport across the Air Space-capillary Barrier

建立一种表面荧光技术测量离子在小鼠离体灌注肺肺泡和毛细血管间的转运。

To develop a pleural surface fluorescence method to measure ion transport in perfused mouse lungs .

重症肺炎造成肺泡壁毛细血管网毁损，红细胞经过时遭到机械性损害；科学技术对于生态环境的破坏越来越明显和严重。

In acute stage of severe pneumonia , the capillary vessels of patient ' pulmonary were damaged , which induced the erythrocytes were destroyed mechanically .

肺泡壁毛细血管充血扩张，有肺透明膜形成。肺间质、肺泡腔内有大量炎性细胞浸润，治疗组以上损伤程度明显减轻。

Blood capillary of alveolar wall engorgement and pulmonary hyaline membrane are formed , and the infiltration of inflammatory cells in alveolar spaces . In the treatment group , these changes were less obvious , and the amplitude decreased .

本实验肺水肿组存活率为零，肺系数为7.56±1.55，镜下见肺泡壁毛细血管扩张，肺泡腔内充满水肿液；

The pulmonary edema group all died within 10 minutes after AD injection , the survival rate being zero and the pulmonary index ( PI ) 7.56 ± 1.55 . The alveoli filled with fluid and ecchymosed hemorrhage could be seen under the light microscope ( LM ) .

经病理检查发现：①小鼠肺泡间隔中毛细血管腔内广泛存在着HAP的聚合体，并有广泛的肺泡间隔内淤血及肺泡水肿；

The pathological examination indicated that : ① There was large quantities of embolism of HAP combined corps obstructed in the capillary vessels of lung , and the alveolar interval congestion and alveolar edema were found extensively ;

照射5个月时，肺组织纤维化明显，间质结构消失代之以纤维和胶原组织，肺泡腔狭窄，毛细血管壁增厚，以b组最为明显。

Five months after Irradiation , pulmonary fibrosis Obviously , the structure disappeared replaced by interstitial collagen fibers and collagen organizations , alveolar space was narrow , capillary wall thickening , Group b is the most obvious . 4 .