爆炸冲击波对单层肺微血管内皮细胞通透性的影响

采用不同压力梯度爆炸冲击波对培养单层肺微血管内皮细胞滤膜作用的模型,观察了不同压力梯度爆炸冲击波对培养的肺微血管内皮细胞单层通透性的影响。结果表明,电导法测定时,100kPa左右的爆炸冲击波压力作用即可见到单层内皮通透性的显著增加;轻度爆炸冲击波的损伤主要以内皮细胞间隙的增加为主要类型,而中强度以上的爆炸冲击波损伤,则主要以内皮细胞的脱落性损伤为主。     

减压病时动物肺微循环和血管变化的研究

用微循环显微镜TV录像系统、肺血管和肺泡ABS铸型方法,以及肺组织学光镜和电镜超微结构研究,探讨了家兔减压病时肺微循环和肺组织损伤的情况,以及球结膜微循环的变化。此外,还应用本所新研制的超声     

大鼠液压冲击脑损伤急性肺水肿的病理观察

我们研究于脑损伤后大鼠急性肺水肿的肺微循环改变.用显微观察方法(H.E、透射电子显微镜)观察液压冲击脑损伤大鼠出现急性肺水肿的肺微循环改变情况.其结果为光镜下肺泡腔有富含蛋白的液体,并有局灶性的出血区,可见透明膜、白细胞及其他组织碎片.电镜下见Ⅰ型肺泡上皮明显肿胀,线粒体肿胀、嵴消失,内质网扩张,Ⅱ型细胞的板层体消失;基底膜肿胀;在出血区多数毛细血管肺泡呼吸膜严重破坏,有严重的不可逆性细胞损伤;肺毛细血管壁松散、断裂、出血及大量血浆蛋白颗粒渗出.结论为液压冲击脑损伤大鼠神经原性肺水肿与脑损伤后肺微循环病理改变有密切关系.     

TNF-α引起的微血管内皮细胞功能障碍及其细胞分子机制

血管内皮细胞是肿瘤坏死因子 (ＴＮＦ α)作用的靶细胞之一。由ＴＮＦ α引起的血管内皮细胞损伤在很多心脑血管疾病和血栓性疾病的发病中具有重要意义。本工作主要研究不同浓度的ｒｈＴＮＦ α(简称ＴＮＦ)引起微血管内皮细胞功能、代谢的早期损伤以及其与微血管内皮细胞中原癌基因和凋亡相关基因表达的关系 ,试图从中说明ＴＮＦ引起微血管内皮细胞功能障碍的表现及其部分细胞分子机制。实验是在体外培养的第二代大鼠肺微血管内皮细胞(ＲＰＭＶＥＣ ,简称内皮细胞 )中进行的。细胞经光镜、电镜的形态观察 ,ｖＷＦ免疫组化阳性 ,ＣＤ3 1免疫…     

实验性减压病时肺微循环变化的研究

本文介绍了家兔减压病时肺微循环和微血管的变化。实验观察到,减压病时动物肺微血管有大小不一的气泡栓塞,血管内膜损伤、内皮细胞间隙增大、血浆外溢,毛细血管中红细胞呈棘状改变。肺Ⅱ型细胞板层体明显增多、内容物聚集及排空,细胞核变形。ABS铸型发现,减压病时肺泡腔严重充盈缺损,表明有渗出物存在。实验结果提示,减压病时动物机体不仅有气泡栓塞,而且亦有肺微循环功能改变以及细胞结构的损害,这种病理学改变无疑影响肺正常气体交换和细胞代谢功能,进而加重减压病的病程。     

兔胸腹部爆炸伤后不同器官微血管通透性的变化

目的探讨爆炸性冲击伤后不同组织器官微血管通透性变化的特点及其可能的机理。方法采用雷管对兔的爆炸性冲击损伤模型 ,以及 125I-白蛋白标记的方法 ,观察爆炸性冲击波对兔心、脑、肺、肾、肝组织中的微血管通透性的影响。结果距爆源20cm处的爆炸冲击波平均压力峰值为174 .4kPa,可引起红细胞压积增加为14.9 % (与对照组相比 ) ,血浆丢失为对照的5.12倍 ;距爆源10cm时 ,爆炸冲击波的压力峰值可陡增至1000kPa以上 ,所致白蛋白漏出率为伤前的1.5倍 ,心、脑、肺、肾组织中的残留放射性较对照组增加约1 .6～1.9倍。结论爆炸冲击波能引起红细胞压积明显增加 ,血浆丢失 ,以及心、脑、肺、肾组织中微血管通透性的增加。     

缺血再灌注肺脏超微结构变化的电镜观察

目的　观察研究新西兰兔肺缺血 再灌注 (ischemic-reperfusion ,I R)过程肺毛细血管及肺泡上皮细胞超微结构变化。方法　取用新西兰兔I R模型的肺组织 (正常组、缺血 1h、再灌注 0 5h和再灌注 2h ,共 4组 )制作常规电镜标本 ,在透射电镜下进行观察。结果　缺血 1h肺毛细血管和肺泡上皮开始发生病理学变化 ,缺血后再灌注 0 5h时 ,结构明显损害 ,再灌注 2h后 ,毛细血管与肺泡结构均开始表现出损伤的修复趋势。结论　肺I R状态下 ,毛细血管内皮细胞和肺泡上皮细胞形态结构上的异常是导致肺功能障碍的病理学依据。     

灵芝对体外培养的微血管内皮细胞增殖和凋亡的影响

目的研究不同剂量灵芝对体外培养的大鼠肺微血管内皮细胞的增殖与凋亡的影响。方法在体外培养肺微血管内皮细胞中做细胞增殖曲线 ,用流式细胞仪分析细胞周期及细胞凋亡的变化。结果培养中加入灵芝 (2.75mg/ml)后第4d开始细胞增殖 ,第7d达高峰(与阴性对照比 )。流式细胞仪分析 ,各剂量组G2-M期细胞明显增多 (与阴性对照比 ) ,但细胞凋亡百分率无显著变化。结论灵芝能促进体外培养的肺微血管内皮细胞增殖作用 ,此作用对保护内皮损伤、加速内皮修复有重要作用     

兔胸腹部爆炸伤后的血液浓缩与肺微血管通透性改变

目的：探讨爆炸冲击伤后血液浓缩的特点及微血管通透性的变化。方法：采用雷管对兔的爆炸性冲击损伤模型与[¹²⁵I]-白蛋白标记的方法，观察爆炸性冲击波对兔肺微血管通透性的影响。结果：距爆源20 cm处的爆炸冲击波压力平均峰值为174.4 kPa，红细胞压积的增加为14.9%，白蛋白漏出率为伤前的1.3倍，左肺组织中残留放射性较对照组增加约18%。结论：100 kPa以上的爆炸冲击波能引起红细胞压积与肺组织中的残留放射性的明显增加。     

微血管内皮细胞的原代培养

本期“改良肺微血管内皮细胞原代培养技术及细胞鉴定”参考文献12：时全星,孙新,李娟,等．微血管内皮细胞的原代培养[J]．现代生物医学进展,2010,10（19）：3609—3612．本文利用大鼠肺组织的原代培养方法（组织块贴壁法）获得肺微血管内皮细胞（PMVECs）。作者通过改进组织块培养时间、培养液中血清的浓度以及培养瓶的材质等措施,经光镜和电镜扫描观察细胞形态、Ⅷ因子抗原检测进行细胞鉴定,PMVECs细胞生长速度和纯度都比较高,改良后的组织块培养方法简单、快捷、有效。     

过氧亚硝基阴离子致大鼠肺微血管壁通透性增高的研究

目的:探讨过氧亚硝基阴离子(ONOO^-)对肺微血管内皮屏障功能的影响和在急性肺损伤发生中的意义。方法:向SD大鼠气管内推注不同浓度的ONOO^-、分解 ONOO^-或溶剂2 h后,检测肺微血管壁通透性变化和肺组织病理学变化,并检测ONOO^-引起正常肺匀浆MDA含量变化。结果: ONOO^-推入气管后,肺系数、肺湿干重比以及肺含水量和伊文思兰含量明显增高呈现剂量效应关系;并可导致肺泡明显萎陷、肺泡壁毛细血管明显扩张充血及局灶性出血,内皮细胞肿胀、核深染及脱落。ONOO^-造成正常肺匀浆MDA含量增加。 结论: 外源性ONOO^-气管推注后可导致明显的肺微血管内皮屏障功能障碍,提示肺内源性ONOO^-生成增多时可能参与介导急性肺损伤的发生。     

山莨菪硷(654-2)预防大鼠实验性肺水肿的电镜观察

静脉注射肾上腺素可造成大鼠致死性肺水肿,这种水肿类似临床上的中枢性肺水肿,属于混合性肺水肿。既有肺毛细血管压力升高,又有肺毛细血管通透性增高。用中药山莨菪碱进行预防效果十分明显。电镜观察提供了这种预防效果的超微结构基础。水肿组内皮细胞及肺泡上皮细胞膨隆,水肿,部份细胞从基底膜脱落,基底膜裸露或断裂。间质腔及肺泡腔充满富含蛋白的水肿液。而预治组病变明显减轻,水肿液明显减少。内皮细胞及上皮细胞基本正常。间质、肺膈增宽,结缔组织增生。这是由于动物存活半个月,炎症被吸收有关。实验表明,山莨菪碱可以明显抑制血管通透性的增高。     

Endothelial nitric oxide synthase expression in pulmonary capillary hemangiomatosis

Pulmonary capillary hemangiomatosis (PCH) is an unusual disorder characterized by the proliferation of capillaries in the alveolar septa and pulmonary interstitium. Originally conceived as a primary idiopathic disorder of the pulmonary microcirculation, recent studies have demonstrated that PCH may be associated with other pathologies. Nitric oxide (NO) is a gaseous free radical with protean biological effects that is released during the intracellular conversion of arginine to citrulline. Nitric oxide synthases (NOS) mediate the production of NO and the release of NO in the microvasculature is specifically catalyzed by endothelial NOS (NOS-III). As NOS contributes to angiogenesis and is reduced in the hypertensive pulmonary microcirculation, we examined the expression of NOS-III protein in situ in the lungs of patients with PCH. Reduced microvascular expression of NOS-III protein by endothelial cells was observed in 4/6 (67%) cases of PCH, and all of these showed concomitant pulmonary vascular hypertensive remodeling. In 2/6 (33%) cases of PCH with no morphologic evidence of pulmonary hypertensive arteriopathy, endothelial expression of NOS-III protein was judged to be either minimally reduced or normal. These findings suggest that NOS-III is specifically reduced in PCH when pulmonary arterial hypertensive remodeling is concomitantly present.     

Ultrastructural Alterations in Canine Lung Allografts

Morphologic alterations in transplanted dog lungs undergoing acute rejection were studied with the electron microscope. Earliest changes were swelling of the type I alveolar cells and cytoplasmic vacuolization in the capillary endothelial cells. Later, there was progressive infiltration of macrophages which contained large osmiophilic inclusions. Type II alveolar cells increased in number and showed vacuolization, fraying and membrane disruption of their lamellar inclusions. A decrease in the relative number of type II cell inclusions and extensive endothelial damage were observed in preterminal biopsies. The significance of these cellular changes in relation to pulmonary rejection requires further investigation.     

Pulmonary interstitial edema and hyaline membranes in adult burn patients. Electron microscopic observations

Pulmonary insufficiency has become a major problem in the care of patients with extensive cutaneous burns and other forms of trauma. Although a variety of pathological changes have been described in the lungs of such patients, probably the most common underlying lesion is interstitial edema with the development of hyaline membranes. Previous light microscopic investigations have shown that interstitial edema with hyaline membrane development is a nonspecific pulmonary reaction that occurs in many conditions and in response to a variety of stimuli. In this study, postmortem electron microscopic observations on the lungs of six burn patients with the lesion are described. Interstitial edema of the alveolar wall was marked and involved primarily the thick portion of the air-blood membrane. The thin portion of the membrane, where epithelial and endothelial basement membranes are normally in close proximity, did not demonstrate accumulation of edema fluid. There was widespread necrosis of the alveolar epithelium. Cellular debris from necrotic alveolar epithelium and fibrin-like material formed a layer that corresponded to the hyaline membranes observed by light microscopy. Hyaline membranes occurred both with and without edema of the underlying interstitium, seemingly indicating that interstitial edema per se was not solely responsible for the epithelial necrosis and resulting hyaline membranes. Evidence of alveolar epithelial regeneration was also found. The regenerated cells had the appearance of type II alveolar cells (granular pneumocytes), which are thought to be the reserve cells of the alveolus. Changes in the alveolar capillaries were minimal. This was a surprising finding, since changes in the interstitium suggested an altered capillary permeability. However, the possibility that endothelial injury had occurred early in our patients and was repaired by the time of their demise could not be ruled out. Futher ultrastructural studies are needed to describe the sequential development of the lesion and to compare the trauma-related lesion with the interstitial edema-hyaline membrane pattern in other clinical and experimental settings.     

Morphology of noncardiogenic pulmonary edema induced by Perilla ketone in sheep.

A single infusion of Perilla ketone (PK) into sheep causes marked increases in lung fluid and solute exchange in the absence of any alteration in either pulmonary arterial or left atrial pressures. These alterations are most compatible with increased pulmonary microvascular permeability. The present paper describes the morphologic changes that accompany the previously described alterations in lung function. In five anesthetized open-chest sheep, lung biopsy tissue was taken at baseline and at 15, 30, 60, 120, and 180 minutes after the start of a single infusion of PK (15-20 mg/kg given over a 20 minute period). Biopsy tissue was taken from different lobes of the lung in random sequence, fixed, and processed for light and electron microscopic examination. Three control sheep received the vehicle, dimethyl sulfoxide, alone. Just 15 minutes after the start of PK infusion, alveolar capillary congestion, accumulation of peripheral lung neutrophils, and intraalveolar and interstitial edema were apparent. Electron microscopy revealed early evidence of damage to both the microvascular endothelial cells and Type I pneumonocytes. The damage became more severe with time. From 30 minutes, occasional nonciliated cells in the airway epithelium exhibited dilated rough and agranular endoplasmic reticulum. Thus, PK causes rapid onset of pulmonary edema accompanied by structural evidence of damage to the microvascular endothelium and Type I pneumonocytes. Pulmonary inflammation was also evident. These structural changes occur before the described alterations in either pulmonary microvascular permeability or reduction in pulmonary compliance.     

电离辐射对内皮细胞和淋巴细胞粘附特性的影响

从电离辐射对微血管内皮细胞和淋巴细胞粘附力影响的角度进一步探讨辐射致微循环损伤的机制。方法：采用细胞粘附观察记录装置，观察不同剂量电离辐射作用对培养的内皮细胞和外周血淋巴细胞粘附特性的影响。结果：不同剂量γ射线（60Co）辐射作用内皮细胞（10、15Gy）或淋巴细胞（3、5Gy）后，二者的粘附特性分别发生了明显的改变，表现为二种细胞间的粘附数量明显增多。结论：电离辐射作用下微循环的损伤性变化可能与内皮细胞和淋巴细胞的粘附特性改变有关。     

Endotoxin enhancement of lymphocyte adherence to cultured sheep lung microvascular endothelial cells.

The most common predisposing factor for development of the adult respiratory distress syndrome is gram-negative sepsis. Our previous studies have shown that a single infusion of Escherichia coli endotoxin into sheep causes early sequestration of lymphocytes in the lungs' microcirculation. In this report, we examined the effects of endotoxin on sheep lymphocyte adherence to sheep pulmonary microvascular endothelial cells in vitro. Endothelial cells were exposed to endotoxin, and subsequent adherence of 51Cr-labeled lymphocytes was measured in a monolayer adhesion assay. Endotoxin enhanced adherence of lymphocytes isolated from blood and caudal mediastinal node (CMN) lymph in a time- and dose-dependent manner. Adherence of CMN lymphocytes increased from a control value of 13.6 +/- 1.6% to 29.9 +/- 3.1% after 4 h of treatment with 1 microgram/ml endotoxin. Both B and T lymphocytes contributed to the increased adherence. Pretreatment of the endothelial cells with cycloheximide revealed that the endotoxin-enhanced adherence was partially dependent upon protein synthesis. Morphologic studies revealed that enhanced adherence was accompanied by a 5-fold increase in migration of lymphocytes between endothelial cells. In contrast to human umbilical vein endothelial cells, antibodies to the known lymphocyte adherence molecules, lymphocyte function-associated antigen (LFA-1), CD-44, and the lymphocyte homing receptor (LECAM-1), were ineffective in blocking adherence to the sheep pulmonary endothelial cells. We conclude that the acute sequestration of lymphocytes in the pulmonary microcirculation of sheep after endotoxin administration is due to increased adhesive properties of the endothelial cells. Our data suggest that this adherence is mediated by as yet undescribed mechanisms that may be unique to pulmonary microvascular endothelium.     

Application of linear integration in the morphometric study of mild and severe pulmonary alveolar injury

In this study we applied linear integration morphometry to characterize the pulmonary alveolar reaction to toxic injury and to study possible relationships between the major tissue and cell compartments of alveolar tissue, normal and injured. Acute alveolar injury of mild and severe intensity was induced in Swiss-Webster mice by the ip administration of the chemicals diquat (4 mg/kg) and butylated hydroxytoluene (BHT; 400 mg/kg). Animals were sacrificed at Days 1 and 2 after diquat treatment and at Days 1, 3, and 5 after BHT treatment. Sampling and analysis of alveolar tissue were conducted at both levels of light and electron microscopy. Thickness distributions of arithmetic and reciprocal intercepts, as well as the arithmetic (tau) and harmonic (tau h) mean thicknesses, were established for the following alveolar compartments: septum, alveolo-capillary barrier (ACB), type I and total epithelia, capillary endothelium, and interstitium. A relative measure of the pulmonary diffusion capacity and the capillary load of alveolar septa were also determined. The parameters calculated from these thickness distributions, such as their slopes, percentages of thin intercepts, and tau/tau h ratios, proved very sensitive and useful in the detection and characterization of morphological alterations in the type I epithelial and capillary endothelial cells following either mild or severe alveolar injury. The epithelial, endothelial, and interstitial layers of pulmonary septa were all characterized by their own pattern of structural changes, so that it proved impossible to relate them in a simple way to the tissue reaction, which can be easily studied at the light microscopic level. Linear integration morphometry thus proved very useful as a morphometric approach to the study of pulmonary alveolar injury and repair.