跨骺钢板固定一定周期取出：继续观察一段时间后骺板的生长抑制情况

文题释义： 骨骺损伤：骺板软骨细胞共分为4层,骨骺损伤后骺软骨的结构发生了一系列修复重建性改变,其中骺板软骨增生层和肥大细胞层的细胞增生、分化、代谢活跃。由于肥大细胞层细胞增大,基质稀少,形成了骺板中最薄弱部位,故受到压力时变化最为显著。 骺板厚度变化率：为随着时间延长,骺板厚度逐渐增加,单位时间内骺板厚度增长的比率。主要是指不同时间节点,骺板厚度生长变化情况。用于观察跨骺板钢板内固定一段时间,取出内固定物后骺板厚度的生长变化情况。 背景：临床上儿童干骺端、骺板周围骨折比较常见,跨骺板钢板内固定对稳定骨折有较为重要的作用。但内固定一定周期后取出内固定物,继续观察一定时间骺板的发育恢复情况鲜有报道。 目的：设计骺板周围骨折动物模型,分析跨骺板置入锁定钢板一定周期取出钢板,继续观察一段时间后骺板的生长抑制情况。 方法：建立32只幼兔右股骨远端骺板上方5 mm骨折模型,随机分4组,每组8只。应用相同型号钢板和螺钉,跨骺板周围骨折线行钢板置入内固定。术后2,4,8,12周取出内固定物,继续观察2周处死幼兔。取出股骨标本,测量股骨长度;作病理切片,测量骺板厚度及肥大细胞计数;观察形态学中肥大细胞及骺板厚度变化情况。将骨折模型作为实验组,以左股骨远端骺板作为对照。 结果与结论：①实验组在内固定2周后,取出钢板继续观察2周,股骨长度、骺板厚度、肥大细胞计数等与对照组对比,差异无显著性意义;②实验组内固定4,8,12周,取出钢板继续观察2周,与对照组相比,实验组股骨长度、骺板厚度、肥大细胞计数等指标未能完全恢复至正常,差异有显著性意义(P < 0.05);③结果表明,在内固定物不伤及骺板的前提下,跨骺板钢板内固定初期(≤2周)取出钢板继续观察2周,适当压力作用对骺板生长发育未产生显著影响;④但持续过久压力限制时(≥4周),内固定对骺板压力限制时间过长,虽然也及时取出内固定,但肢体长度、骺板厚度、肥大细胞计数等指标均未能完全恢复正常,可导致骺板生长部分或者完全阻滞,引起肢体畸形及骺板发育停滞。 ORCID: 0000-0003-2448-9683(崔庆达) 中国组织工程研究杂志出版内容重点：人工关节;骨植入物;脊柱;骨折;内固定;数字化骨科;组织工程     

不同部位贯穿伤对骺板生长发育影响的实验研究

目的探讨骺板不同部位损伤对骺板生长发育的影响。方法选用新西兰白兔96只,估算骺板损伤面积百分比,随机分组制备股骨远端骺板中央及外侧边缘区损伤模型,术后不同时间从大体和组织学观察骺板发育情况。结果直径2.0mm、3.0mm和3.5mm组骺板损伤面积百分比分别为（3.33±0.42）%、（6.77±0.23）%和（9.05±0.30）%。术后骺板中央区损伤3.0mm组和3.5mm组出现生长阻滞,而外侧边缘区损伤3.5mm组出现生长阻滞 外侧边缘区损伤3.0mm组和3.5mm组出现髁部发育阻滞及外翻成角畸形。组织学观察发现骺板损伤区骨桥形成,软骨细胞呈“岛状”分布,排列不规则,周围被骨桥包绕。结论骺板发育阻滞与损伤面积百分比有关,中央区损伤主要引起肢体短缩畸形,而外侧边缘区损伤主要引起肢体成角畸形及骺板横向发育阻滞 骺板损伤后其损害是永久性的 骺板损伤后软骨细胞修复能力有限。     

人窦房结胶原纤维网架的构筑-NaOH蚀刻／扫描电镜观察

为研究人窦房结胶原纤维网架的三维构筑及其与窦房结中央动脉的关系，用NaOH销蚀法扫描电镜观察了11例成人窦房结。研究表明，成人窦房结的胶原纤维网架致密，窦房结中央动脉穿过结的中央或一侧。窦房结中央动脉的胶原纤维支架分为三层：在内膜呈网状；中膜的胶原纤维形成胶原纤维小梁，在中膜内层，胶原纤维小梁围绕窦房结中央动脉排列，在中膜外层，     

兔股骨骺板生长与阻滞压力关系式的探讨

本文用三组压力固定模式的预压值对兔股骨骺板加压，测试阻止兔骺板生长的阻滞压力，以指数函数表达骨骺板生长时间的关系，由此得到二者的关系方程。     

骺板移植的实验形态学观察

实验研究将３￣５月龄幼狗１２条分为二组进行右侧腓骨上端骨骺游离原位再植。一组为带血管骺板移植，另一组为不带血管骺板移植。经组织学及超微结构观察表明，带血管移植的骺板的形态学表现与正常对照侧相似，而不带血管移植的骺板则变性、坏死和吸收。从而证实了骺板移植须有血供存在，也证实了带血管骺板移植具有临床应用潜力。     

内毒素性DIC与幼兔多发性骨坏死关系的实验研究

本研究用２０只纯种日本大耳白幼兔，实验组连续二次、间隔２４ｈ经静脉注入纯制大肠杆菌内毒素（１００μｇ／ｋｇ），建立革兰氏阴性菌败血症休克模型，二周末处死，以９９ｍＴｃ－ＭＤＰ骨显像法及病理学检查观察模型动物骨骼系统改变情况，评价ＤＩＣ过程对骨骼系统的影响。结果发现，在第二次静脉注射内毒素一周后，实验组动物长骨骨端血流量计数对比值显著下降，二周末病理检查，证明出现了多发性骨坏死，并集中地发生在长管状骨骨端，分别为股骨髁、肱骨头、胫骨上端、股骨头及尺骨近端。病理表现为骺及干骺端侧髓腔内骨髓细胞坏死，以及骺板干骺端侧的软骨细胞柱、新生及成熟骨小梁的坏死崩解。部分动物有整块骺板的变性及坏死。实验发现，骨坏死的发生和分布，与骨微循环结构的破坏密切相关。这表明，内毒素及其引发的ＤＩＣ反应可以破坏骺区的骨微循环系统，引起幼兔全身多发的以骺板为中心的骨坏死。本研究提示，内毒素及其引发的ＤＩＣ过程可能是严重革兰氏阴性菌败血症后，儿童后遗骨发育障碍的重要原因     

糖尿病早期角膜组织的超微变化

目的 :了解早期糖尿病角膜组织的超微变化 ,探讨糖尿病角膜病变的发病机制。方法 :选取SD雄性大鼠 4 0只 ,随机分为糖尿病组和正常对照组 ,前者以链脲佐菌素诱导成糖尿病模型。分别于 6、8、10、12周取角膜 ,扫描电镜及透射电镜下观察其超微改变。结果 :各个观察时点糖尿病大鼠角膜上皮和内皮细胞水肿 ,胞浆内线粒体增多和肿胀 ,随着病程进度而明显 ;角膜内皮的破坏从周边开始 ,逐渐向中央发展 ;成模后第 10周开始出现基质层胶原纤维排列紊乱 ,部分呈格子状排列 ,有断裂现象。结论 :糖尿病性角膜病变超微结构的改变导致了角膜功能异常 ,这可能与高血糖时物质代谢异常有关。     

糖尿病早期角膜组织的超微变化

目的:了解早期糖尿病角膜组织的超微变化,探讨糖尿病角膜病变的发病机制。方法:选取SD雄性大鼠40只,随机分为糖尿病组和正常对照组,前者以链脲佐菌素诱导成糖尿病模型。分别于6、8、10、12周取角膜,扫描电镜及透射电镜下观察其超微改变。结果:各个观察时点糖尿病大鼠角膜上皮和内皮细胞水肿,胞浆内线粒体增多和肿胀,随着病程进度而明显;角膜内皮的破坏从周边开始,逐渐向中央发展;成模后第10周开始出现基质层胶原纤维排列紊乱,部分呈格子状排列,有断裂现象。结论:糖尿病性角膜病变超微结构的改变导致了角膜功能异常,这可能与高血糖时物质代谢异常有关。     

NaOH消蚀法制备胎儿脱细胞真皮基质的研究

目的：探索NaOH消蚀法对胎儿真皮基质的成分及其形态结构的影响。方法：使用NaOH消蚀法制备胎儿皮肤的脱细胞真皮基质(ADM)，应用组织化学和免疫组织化学染色方法检测细胞的余留及细胞外基质成分的破坏情况，应用扫描电镜观察ADM的构筑。结果：NaOH消蚀处理16h即可去除真皮细胞成分。制备的ADM韧性好，勿需戊二醛交联。弹性纤维的含量有所减少而胶原纤维形态完整，排列正常，保留了基本的真皮构筑。HLA—DR呈阴性，Fibronectin(FN)呈弱阳性，Laminin(LN)和Ⅳ型胶原均呈阴性。结论：NaOH消蚀法简易经济，去除细胞成分较彻底，所制备的ADM韧性好，胶原纤维形态完整，排列正常，但对基膜的成分及结构破坏较重。     

碱性成纤维细胞生长因子对离心管内培养骺板细胞生成软骨组织的作用

背景：采用离心管技术体外培养骺板细胞的报道已很多。 目的：观察碱性成纤维细胞生长因子对离心管内培养的骺板细胞生成类骺板组织的影响。 方法：获取3周龄新西兰白兔股骨远端的骺板组织,利用组织块纱巾培养法获得骺板细胞,加入含有10 μg/L碱性成纤维细胞生长因子的DMEM培养液,连续培养4周。 结果与结论：离心管内聚集的骺板细胞在含有碱性成纤维细胞生长因子的DMEM培养液中形成类骺板样组织块。在组织块外周形成类似骺软骨的生发层,中心的骺板细增殖情况良好,向肥大细胞方向分化。类骺板样组织甲苯胺蓝及番红“O”染色阳性,Ⅱ型胶原免疫组织化学染色呈强阳性。说明碱性成纤维细胞生长因子能够促进离心管中的骺板细胞形成富含蛋白聚糖及Ⅱ型胶原等细胞外基质的类骺板样软骨组织。     

髋关节软骨高、低负重区微纳结构的力学性质对比

文题释义：微纳层面：相对于宏观层面而言,是对宏观层面的一个补充,由肉眼可见的毫米级别到肉眼不可见的微米、纳米级别。分别使用微米级、纳米级原子力显微镜探针测量软骨微纳弹性模量,以揭示软骨在微纳层面力学性能的特点,以及与宏观层面力学性能的关系。 负重区：在日常活动运动中,由于机体力线等不同,势必造成软骨不同区域负重出现不同,不同的负重也会影响到胶原纤维等物质的重塑重构,引起软骨力学性能的改变。 背景：髋关节软骨具有高、低负重区域,既往研究表明2个区域的宏观弹性模量是不同的。然而在微米和纳米水平上的弹性模量尚不清楚,这些信息对于进一步理解软骨微米和纳米力学性质至关重要。此外,影响软骨2个区域机械性能的微纳结构至今仍有待阐明。 目的：探究微纳层面髋关节软骨高、低负重区力学性质与结构。 方法：取新鲜正常猪股骨头软骨,使用原子力显微镜直径为5 μm的球形尖端测量不同负重区微米级压缩弹性模量,使用曲率半径为5 nm的ScanAsyst-Air探针测量其纳米级压缩弹性模量、纳米结构和胶原纤维直径。扫描电子显微镜用于识别软骨不同负重区微米结构。 结果与结论：①股骨头软骨高负重区微米级弹性模量为(433.05±146.52) kPa,低负重区微米级弹性模量为(331.19±84.88) kPa,高负重区域在微米水平上的压缩弹性模量显著高于低负重区域(P=0.029 8);②股骨头软骨高负重区纳米级弹性模量为(1.24±0.42) GPa,低负重区纳米级弹性模量为(1.28±0.41) GPa,在纳米水平上2个区域的胶原纤维的压缩弹性模量差异无显著性意义(P=0.846 2);③在微米水平上,股骨头软骨高负重区域的胶原纤维排列更规则;在纳米水平上,2个负重区域的胶原纤维直径差异无显著性意义(P=0.926 4);④以上结果表明,股骨头软骨高负重区胶原纤维较低负重区交联更规则,使软骨高负重区微米级压缩弹性模量高于低负重区,与宏观上压缩弹性模量趋势一致,但高负重并没有影响到纳米层面单个胶原纤维。 ORCID: 0000-0001-7971-5372(郭江博) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

Nanomechanical characterization of micro/nanofiber reinforced type I collagens

To function properly in the rigorous tissue environment, implanted scaffolds for tissue engineering are required to meet certain standards of strength and mechanical integrity. However, the soft nature and moisture condition of biomaterials impose great challenges to many existing techniques and instrumentations for measuring their mechanical properties at micro/nano scale. In this work, we demonstrate the testing methodologies of micro/nano fiber reinforced type I collagens, and obtain basic mechanical property data of two types of modified collagens-micro carbon fiber reinforced collagen (MCFR) and nano collagen fiber reinforced collagen (NCFR). Results show that mechanical properties of collagen tissues can be enhanced by reinforcing nano collagen fibers but weakened by micro carbon fiber reinforcements. Mechanisms are discussed on how natures of reinforcing fibers affect reinforcement to the collagen matrix, as well as how reinforcements behave within the collagen matrix in response to mechanical strain.     

The three-dimensional ultrastructure of the collagen fibers, reticular fibers and elastic fibers: a review]

Fibrous components of the connective tissue are light-microscopically classified into three types: collagen fibers, reticular fibers and elastic fibers. The present paper reviews the three-dimensional ultrastructure of these fibrous components, mainly based on our studies by scanning electron microscopy. The collagen fibers are shaped like tapes or cords about 1 to 20 microns in diameter. Each fiber is a bundle of fibrils running roughly parallel to each other. These collagen fibrils vary in diameter from 30 to 300 nm depending on their locating area of the body, and show a repeating pattern of depressed and protruding segments on the surface. The reticular fibers consist of collagen fibrils about 20-40 nm in diameter, which run singly or in small bundles. They are usually interwoven elaborately to form thin lace-like sheets or sheaths attaching to basal laminae of such cells as epithelial, endothelial and muscular cells. These fibers are considered to play an important role not only in adhering the cells to the collagen fibers, but also in constituting the skeletal framework suitable for individual cells and tissues. The elastic fibers consist of two different components: elastin and fibrillin. Elastin forms unit fibrils of 0.1-0.2 micron thickness which are arranged in bundles or laminae specific to individual organs and tissues. Fibrillin, on the other hand, forms microfibrils about 10 nm in diameter running in or along elastin bundles. These microfibrils also form delicate networks separate from elastin components. For a comprehensive understanding of the fibrous components in the connective tissue, the author proposed categorizing them into two systems: the collagen fibrillar system as a supporting framework of tissues and cells, and the fibrillin-elastin fibrillar system for distributing stressing forces uniformly in tissues.     

Origins and pathways of fluid entering sublobular lymphatic vessels in cat livers

The liver, which produces a large volume of lymph, has a lymphatic system which can be classified into three categories: portal, sublobular, and superficial lymphatic vessels. As little is known about the origin and pathways of sublobular lymph, this study demonstrates pathways of interstitial fluid flowing into sublobular lymphatic vessels. Livers from cats whose thoracic ducts were either ligated or non-ligated were examined by light-, transmission electron- and scanning electron-microscopy (SEM). Complete ligation of the thoracic duct caused significant dilation of the hepatic sinusoids, the space of Disse, and channels passing through the limiting plate. Sublobular interstitial space and sublobular lymphatic vessels were also expanded. The channels between hepatocytes forming the limiting plate contained collagen fibers, and connected the space of Disse with a sublobular interstitial space. The alkali-water maceration/SEM confirmed that collagen fibers traversing the layer of the limiting plate independently of blood vessels connected collagen fibers in the space of Disse with those in the sublobular space. Complete ligation of the thoracic duct also showed an accumulation of mast cells and plasma cells in the sublobular interstitial space. Our data suggest that fluid in the space of Disse flows along collagen fibers in channels traversing the limiting plate as well as those along the sinusoids and central veins that drain into sublobular veins, and enters the sublobular interstitial space to finally lead into sublobular lymphatic vessels. Our study has also shown that hepatic lymphostasis causes the accumulation of mast cells and plasma cells in the sublobular interstitial space, which may be involved in lymphangiogenesis and fibrogenesis.     

The role of mesenchyme-like tissue in the pathogenesis of thanatophoric dysplasia

We have studied the light microscopic, transmission, and scanning electron microscopic (SEM) findings in 13 cases of thanathophoric dysplasia (TD) and 4 control infants. In the TD growth plate, areas with less abnormal cartilage and bone alternated with areas of severely abnormal cartilage and bone. These latter abnormal areas were always found around tongues of apparent mesenchymal tissue that appeared to penetrate from the investing perichondrium and periosteum. The ultrastructure of the less abnormal areas was similar to that of the control infants, including cell and matrix structure as well as mineralization. The abnormal cartilage and bone had many ultrastructural abnormalities that were also found in the adjacent mesenchymal tissue. The mesenchymal cells, adjacent chondrocytes, and osteoblasts contained dilated endoplasmic reticulum and moderately large intracytoplasmic vacuoles. In the area adjacent to the cartilage, the matrix of the apparent mesenchyme contained thin collagen fibers and proteoglycan granules, whereas the matrix adjacent to the bone contained thick bundles of short collagen fibers. The matrix of the surrounding cartilage and bone resembled the adjacent matrix in the mesenchyme. In addition, many vesicular structures or osmiophilic particles were found in the matrix of the mesenchyme and adjacent cartilage and bone. SEM examination showed normal and abnormal bone trabeculae adjacent to each other. In the abnormal trabeculae, there were large, densely packed osteoblastic and osteocytic lacunae. The calcified collagen fibers had a random orientation, in contrast to the longitudinal orientation in the relatively normal bone. Chemical studies of collagen in the metaphyses of bones from five infants with TD showed a small amount of collagen type III (less than 5%), which was not found in three control infants. Thus, a basic pathogenetic mechanism in the skeletal abnormalities of TD appears to be the focal replacement of the growth plate and periosteum by persisting abnormal mesenchymal-like tissue from which the abnormal bone originates.     

大鼠心肌间质胶原的扫描电镜观察

目的　探讨大鼠心肌间质胶原网络的形态构筑及其功能意义。　方法　利用四氧化锇和氢氧化钠细胞浸渍方法 ,于扫描电镜下对大鼠心肌间质胶原进行观察。　结果　粗细不等的胶原纤维相互交织充填于心肌细胞及毛细血管间。粗胶原纤维平行或斜跨于细胞和血管表面 ,形成粗大的框架式结构 ;细胶原纤维卷曲蓬松 ,呈鞘状包裹心肌细胞和毛细血管 ,相邻的胶原鞘彼此融合形成间隔。　结论　心肌间质胶原网络由粗大的框架式结构和纤细的胶原网组合而成 ,它对维护心肌细胞的正常功能可能有重要的作用     

The connective tissue and glial framework in the optic nerve head of the normal human eye: light and scanning electron microscopic studies

The arrangement of connective tissue components (i.e., collagen, reticular, and elastic fibers) and glial elements in the optic nerve head of the human eye was investigated by the combined use of light microscopy and scanning electron microscopy (SEM). Light-microscopically, the optic nerve head could be subdivided into four parts from the different arrangements of the connective tissue framework: a surface nerve fiber layer, and prelaminar, laminar, and postlaminar regions. The surface nerve fiber layer only possessed connective tissue elements around blood vessels. In the prelaminar region, collagen fibrils, together with delicate elastic fibers, formed thin interrupted sheaths for accommodating small nerve bundles. Immunohistochemistry for the glial fibrillary acidic protein (GFAP) showed that GFAP-positive cells formed columnar structures (i.e., glial columns), with round cell bodies piled up into layers. These glial columns were located in the fibrous sheaths of collagen fibrils and elastic fibers. In the laminar region, collagen fibrils and elastic fibers ran transversely to the optic nerve axis to form a thick membranous layer - the lamina cribrosa - which had numerous round openings for accommodating optic nerve fiber bundles. GFAP-positive cellular processes also ran transversely in association with collagen and elastin components. The postlaminar region had connective tissues which linked the lamina cribrosa with fibrous sheaths for accommodating nerve bundles in the extraocular optic nerve, where GFAP-positive cells acquired characteristics typical of fibrous astrocytes. These findings indicate that collagen fibrils, as a whole, form a continuous network which serves as a skeletal framework of the optic nerve head for protecting optic nerve fibers from mechanical stress as well as for sustaining blood vessels in the optic nerve. The lamina cribrosa containing elastic fibers are considered to be plastic against the mechanical force affected by elevation of the intraocular pressure. The present study has also indicated that glial cells with an astrocytic character play an important role in constructing the connective tissue framework characteristic of the optic nerve head.     

实验性肝纤维化大鼠胶原网络构筑的扫描电镜观察

目的 探讨肝纤维化大鼠胶原网络的三维形态构筑的变化。方法 采用健康雄性Wislar大鼠,随机分为对照组和肝纤维化组,后者采用60％的四氯化碳植物油皮下注射,造成肝纤维化大鼠模型,分别于实验的第10周和12周末取材,作为10周和12周肝纤维化组,行天狼猩红显色,光镜下观察和氢氧化钠浸渍,扫描电镜下观察胶原网络的构筑。结果 扫描电镜下,随着肝纤维化程度的加重,增生的胶原纤维交织成网,分隔包裹正常肝组织,形成大小不等圆形或椭圆型肝组织团块,近似于“蜂窝状”囊性的假小叶结构;相邻假小叶之间的胶原纤维沉积明显,并与包裹门管区和血管的纤维鞘相延续为间隔。与对照组相比,10周肝纤维化组形成了尚不完整的假小叶囊,12周组的小叶囊致密完整。结论 肝纤维化时胶原纤维超微构筑发生了改变,增生的胶原网络主要由粗、细纤维构成。     

Collagen fibers,reticular fibers and elastic fibers. A comprehensive understanding from a morphological viewpoint

Fibrous components of the extracellular matrix are light-microscopically classified into three types of fibers: collagen, reticular and elastic. The present study reviews the ultrastructure of these fibrous components as based on our previous studies by light, electron, and atomic force microscopy. Collagen fibers present a cord- or tape-shape 1-20 microm wide and run a wavy course in tissues. These fibers consist of closely packed thin collagen fibrils (30-100 nm thick in ordinary tissues of mammals), and exhibit splitting and joining in altering the number of the fibrils to form a three-dimensional network as a whole. Individual collagen fibrils (i.e., unit fibrils) in collagen fibers have a characteristic D-banding pattern whose length is ranges from 64 to 67 nm, depending on tissues and organs. During fibrogenesis, collagen fibrils are considered to be produced by fusing short and thin fibrils with tapered ends. Reticular fibers are usually observed as a delicate meshwork of fine fibrils stained black by the silver impregnation method. They usually underlie the epithelium and cover the surface of such cells of muscle cells, adipose cells and Schwann cells. Electronmicroscopically, reticular fibers are observed as individual collagen fibrils or a small bundle of the fibrils, although the diameter of the fibrils is thin (about 30 nm) and uniform. Reticular fibers are continuous with collagen fibers through the exchange of these collagen fibrils. In silver-impregnated specimens, individual fibrils in reticular fibers are densely coated with coarse metal particles, probably due to the high content of glycoproteins around the fibrils. Elastic fibers and laminae are composed of microfibrils and elastin components. Observations of the extracted elastin have revealed that elastin components are comprised of elastin fibrils about 0.1-0.2 microm thick. Elastic fibers and laminae are continuous with networks and/or bundles of microfibrils (or oxytalan fibers), and form an elastic network specific to individual tissues. The fibrous components of the extracellular matrix are thereby morphologically categorized into two systems: the collagen fibrillar system as a supporting framework of tissues and cells, and the microfibrilelastin system for uniformly distributing stress to maintain the resilience adapted to local tissue requirements.     

腺苷A2A受体基因敲除小鼠瘢痕胶原亚型的变化

背景：作者前期研究发现腺苷受体激动剂可以刺激胶原合成,腺苷受体拮抗剂可以抑制胶原合成,并且可以减轻皮肤胶原纤维增生。腺苷A2A 受体基因敲除小鼠瘢痕转化生长因子β表达降低。 目的：利用苦味酸-天狼星红偏振光法观察腺苷A2A 受体基因敲除小鼠瘢痕胶原亚型的变化并探讨其机制。 方法：腺苷A2A受体基因敲除小鼠和野生型小鼠制作瘢痕模型,采用苦味酸-天狼星红偏振光法对瘢痕组织中胶原的性质及分布特点进行观察、确定瘢痕组织胶原类型、分布、排列与水平。 结果与结论：偏振光显微镜下可见野生型组小鼠增生性瘢痕组织中含有大量的嗜酸性胶原蛋白纤维束,Ⅰ型胶原纤维为红色,呈致密的条束状,显示很强的双折光性,腺苷A2A 受体基因敲除小鼠瘢痕缺乏粗大胶原束,呈稀疏的条束状,排列相对整齐、密度较为均匀,Ⅰ型胶原纤维水平减少(P < 0.01),瘢痕增生显著减轻。提示腺苷A2A 受体参与瘢痕增生,对预防瘢痕增生有积极意义。