Developing Elastic Tissue: An Electron Microscopic Study

Electron microscopic identification of elastic tissue in normal and disease states has been uncertain due to the lack of a specific electron-dense stain. Recently we introduced a silver porphyrin electron microscopic stain (silver tetraphenylporphine sulfonate) for the identification of adult elastic tissue. This stain has now been employed to study the development of elastic tissue with the aim that new and old elastica can be differentiated at the electron microscopic level. Present observations showed that developing elastica consisted of two distinct morphologic components. Each portion exhibited different staining properties with the silver porphyrin and lead citrate. One component was fibrous and the other amorphous. The fibrous component stained with lead citrate while the amorphous stained with the silver porphyrin. The fibrous component was the first to appear; the amorphous portion appeared later in development and was formed within the fibrous matrix. Mature elastic tissue was devoid of the fibrous component. Based upon the morphologic appearance and staining properties, one can now differentiate between newly formed elastic tissue and the existing one in various disease states.     

Type II pneumocytes are preferentially located along thick elastic fibers forming the framework of human alveoli

Type II pneumocytes were found to be preferentially located on thick elastic fibers which formed the main structural framework of the alveoli in humans. Eight lobes resected from eight patients with adenocarcinoma or atypical adenomatous hyperplasia and two lobes from two necropsies were examined. Four small specimens of normal lung tissue were obtained from each lobe fixed in a buffered formalin. Thick sections (200-300 microm) were stained with hematoxylin to contrast nuclei or with elastica staining to demonstrate elastic fibers and immunostained with an antibody against Thomsen-Friedenreich antigen after pretreatment with sialidase to visualize type II pneumocytes. Alveolar structure and the distribution of type II pneumocytes were examined in 3D reconstructions generated using a standard microscope, a personal computer and NIH-Image software. Nuclei including those of type I and type II pneumocytes and endothelial cells were distributed diffusely throughout the alveolar wall. Thick elastic fibers constructed the main structural framework of the alveoli and formed the sides of the polygonal alveoli. Type II pneumocytes were found to be linearly located along these thick elastic fibers. This previously undisclosed distribution of type II pneumocytes may be concerned with alveolar rapid movement.     

An autopsy case of pseudoxanthoma elasticum: histochemical characteristics

An autopsy case of pseudoxanthoma elasticum is reported. A Japanese female patient complained of yellow papules on the neck, precordium, and axilla, beginning at 54 years of age. When the patient was 58 years old, in response to her visual disturbance a funduscopic examination was performed, revealing angioid streaks, and skin biopsy identified a characteristic pseudoxanthoma elasticum (PXE) lesion. The patient developed congestive heart failure, and following mitral valve prolapse and regurgitation flow into the left atrium, mitral valve replacement with a prosthetic valve was performed when the patient was 65 years old. Soon afterward, the patient complained of gait disturbance, and she died of congestive heart failure at 68 years of age. Autopsy specimen revealed fragmented, granular, and calcified elastic fibers in the middle to deep dermis and in the thickened subendocardium, and small to medium-sized muscular arteries revealed fragmented, laminated, and calcified elastic lamina; vascular changes were seen in the heart, lung, kidney, gastrointestinal tract, and iliac artery. Disrupted elastic fibers were visualized using the Weigert resorcin fuchsin method and were stained positive by antielastin and antifibronectin antibodies. Calcification was confirmed by von Kossa staining. Affected areas were PAS-positive after diastase digestion, indicating the presence of glycoprotein. Affected areas were colloidal iron-positive, indicating the presence of proteoglycan matrix.     

Elastin VII: Aging effects on vascular elastica staining by oil soluble nigrosin dyes

Summary Neutral hydroalcoholic stains with spirit soluble nigrosin (C.I. 50415) and nigrosin base (C.I. 50415B) were applied to a series of human arteries from individuals ranging from newborn to 82 years of age for the demonstration of the selective staining by these dyes of the aging change in their elastica described by Lillie, Pizzolato and Donaldson (1974). The staining is absent in infants and children. It first appears in slight grade in some individuals at age 18. It increases in frequency and intensity with advancing age. It is often seen without obvious other histologic lesion and is regularly present when fibrous and fibroatheromatous plaques appear. In this series it was studied in the aorta of children and in grossly relatively normal areas of the superior mesenteric artery which was selected for the survey because of its usual rather slight involvement in arteriosclerosis. The intensity of the neutral nigrosin staining of the elastica of this artery appeared to be uninfluenced by the extent or severity of aortic lesions in the same individual. This nigrosinophilia appears to be an integral early phase in the development of the arteriosclerotic process and may precede appearance of fibrous or fibroatheromatous plaques by some years. The nigrosinophilia has been assigned (1974) to a lipoprotein alteration of arterial elastica. Prolonged storage in formol in plastic bags induced a strong neutral Solvent black 5 and 7 staining of aortic elastica in the normally negative 10–20 year age group. This reaction is presently considered artifactual, but is being studied further experimentally.Supported by U.S.P.H.S. Grants, NIH HL 08974 and HL 14496 from the National Heart and Lung Institute     

Cartilage formation and calcification in arteries of mice lacking matrix Gla protein

Matrix Gla protein (MGP/Mgp) is a protein expressed predominantly by vascular smooth muscle cells (VSMCs) and by chondrocytes. Transgenic mice lacking Mgp die 1-3 months after birth due to calcification of elastic fibers and rupture of large elastic arteries such as the aorta. Here, we report on cartilage formation that commonly occurs in calcified arteries of Mgp-/- mice. Using histology, von Kossa staining, immunohistochemistry, and Western blotting, together with examination of cellular markers for VSMCs and extracellular matrix markers for cartilage, we provide evidence for cell transformation from VSMC to chondrocyte in the arterial media in the absence of Mgp. At 2 weeks of age in the aorta of Mgp-/- mice, VSMCs lose immunostaining for smooth muscle alpha-actin concomitant with the appearance of cartilage molecules as shown by immunohistochemical staining and Western blotting for aggrecan, link protein, and type II collagen. These data provide evidence that the absence of Mgp, and/or calcification of the ECM, in the arterial media can trigger chondrocyte differentiation and cartilage formation in blood vessels.     

Cartilage Formation and Calcification in Arteries of Mice Lacking Matrix Gla Protein

Matrix Gla protein (MGP/Mgp) is a protein expressed predominantly by vascular smooth muscle cells (VSMCs) and by chondrocytes. Transgenic mice lacking Mgp die 1-3 months after birth due to calcification of elastic fibers and rupture of large elastic arteries such as the aorta [6]. Here, we report on cartilage formation that commonly occurs in calcified arteries of Mgp &#109 / &#109 mice. Using histology, von Kossa staining, immunohistochemistry, and Western blotting, together with examination of cellular markers for VSMCs and extracellular matrix markers for cartilage, we provide evidence for cell transformation from VSMC to chondrocyte in the arterial media in the absence of Mgp. At 2 weeks of age in the aorta of Mgp &#109 / &#109 mice, VSMCs lose immunostaining for smooth muscle &#102 -actin concomitant with the appearance of cartilage molecules as shown by immunohistochemical staining and Western blotting for aggrecan, link protein, and type II collagen. These data provide evidence that the absence of Mgp, and/or calcification of the ECM, in the arterial media can trigger chondrocyte differentiation and cartilage formation in blood vessels.     

Ultrastructural cytochemistry of carbohydrates in microfibrils associated with the amorphous elastin in the monkey aorta

Two distinct ultrastructural components of elastic fibers can be identified--namely, the amorphous elastin and the microfibrils. We have examined the tunica adventitia of monkey aortas to demonstrate differential localization of carbohydrates in elastic fibers and collagen fibrils using Thiéry's periodic acid-thiocarbohydrazide-silver proteinate (PA-TCH-SP) staining of thin sections for vicinal-glycol-containing complex carbohydrates, en bloc concanavalin A (Con A) staining specific for alpha-D-mannosyl and alpha-D-glucosyl groups, and en bloc wheat germ agglutinin (WGA) staining specific for N-acetyl-D-glucosamine, N-acetylneuraminic acid, and N-acetyl-D-galactosamine. The PA-TCH-SP method moderately stained microfibrils and weakly stained collagen fibrils, but did not stain the amorphous elastin. Both Con A and WGA staining methods strongly stained microfibrils and moderately stained collagen fibrils, whereas the amorphous elastin lacked staining. Thus PA-TCH-SP, Con A, and WGA staining methods allow differential ultrastructural localization of carbohydrates in elastic fibers and collagen fibrils in monkey aortic adventitia and demonstrate the presence of more carbohydrate components in microfibrils than in collagen fibrils, whereas amorphous elastin lacks carbohydrate staining.     

Fluorescence, birefringence and confocal microscopy of the abdominal aorta from nonobese diabetic (NOD) mice

In this study, nonenzymatic glycosylation was assessed in aorta extracellular matrix (ECM) from nonobese diabetic (NOD) mice, using nitroblue tetrazolium (NBT). Molecular and structural changes were investigated in elastic lamellae and collagen fibers of diabetic mice aortas after staining with dansyl chloride and anilinonaphthalene sulfonate (ANS). Alterations in arterial autofluorescence and birefringence of collagen fibers were investigated in unstained aortas. Proliferation of smooth muscle cells (SMC) was also investigated by Feulgen reaction staining assessed by confocal microscopy and image analysis. Assessment of nonenzymatic glycosylation demonstrated glycosylation products in the aorta ECM of NOD mice. Elastic lamellae and collagen fibers from NOD mouse aortas presented less intense fluorescence after staining with dansyl chloride and ANS when compared to aortas of control nondiabetic mice. However, unstained NOD aortas showed more intense autofluorescence when compared to controls. Birefringence analysis suggests alterations in the higher molecular packing of the arterial collagen fibers in NOD aortas. In aortas stained by Feulgen reaction, no evidence of SMC proliferation was observed in diabetic aortas.     

Heterogeneity of myosin antigenic expression in vascular smooth muscle in vivo

Rabbit antisera elicited against purified human nonmuscle (platelet) and smooth muscle (uterine myometrium) myosins identified distinct species of myosin when frozen sections of a variety of mammalian tissues were examined by immunofluorescence microscopy. Antiplatelet myosin antiserum specifically stained several nonmuscle cell types including epithelial, some connective tissue, and all vascular endothelial (arterial, venous, capillary) cells. Antismooth muscle myosin antiserum stained only smooth muscle and no other cell types. Neither antiserum reacted with rat cardiac (ventricular) or skeletal muscle cells. Antismooth muscle myosin antiserum staining was detectable in medial vascular smooth muscle in all vessels examined from rat, bovine, human, and guinea pig sources (including elastic and muscular arteries, arterioles, venules, and veins). Although antiplatelet myosin antiserum did not stain nonvascular smooth muscle or vascular smooth muscle in muscular arteries, arterioles, venules, or veins, it did uniformly and specifically stain medial vascular smooth muscle in elastic arteries. This staining of elastic arteries was abolished by absorption of antiplatelet myosin antiserum with purified platelet myosin but not uterine myosin. Similarly, the reactivity of antismooth muscle myosin antiserum was abolished by incubation with uterine but not platelet myosin. The differences in staining patterns observed with antiplatelet myosin antiserum and antismooth muscle myosin antiserum in elastic arteries versus other blood vessels suggests a heterogeneity of antigenic expression in vascular smooth muscle myosin. The most likely explanations for this heterogeneity are the presence of different gene products (myosin isozymes) or a posttranslational alteration (possibly conformational) of a single myosin species. Heterogeneity in this important component of the contractile apparatus of vascular smooth muscle may have significant implications for the physiology and pathophysiology of the vessel wall.     

Abnormal Elastic Fibers in Elastosis of Breast Carcinoma UItrastructuraI and ImmunohistochemicaI Studies

Elastosis in benign and malignant breast lesions was studied by light microscopic immunohistochemistry for elastin and by electron microscopy. Upon immunohistochemical examination for elastin, elastosis, particularly in scirrhous-type ductal carcinoma, showed two characteristic staining patterns: fibrously and intensely stained elastic fibers and evenly stained elastic masses. Elastic fibers showing increased fibrous staining occurred mainly in the stromal areas, and were considered to be newly formed because they consisted of tannic acid-positive amorphous components and abundant microfibrils. Evenly stained elastic masses were observed mainly in the periductal areas and showed less intense stainability. These masses consisted of numerous fine amorphous components with plentiful microfibrils. In some regions within these masses, there were condensed accumulations of irregularly arranged small amorphous components associated with only a few microfibrils. These amorphous components had an ill-defined outline and were occasionally associated with spiralling collagen fibrils and cell debris. On the basis of these findings, the periductal evenly stained elastic masses were thought to be formed by excessive production of elastic fibers and degradation of pre-existing and newly formed elastic fibers. Acta Pathol Jpn 39: 245–253, 1989.     

Ultrastructural distribution of sulfated complex carbohydrates in elastic cartilage of the young rabbit

Sulfated glycosaminoglycans are an integral component of elastic cartilage. We have investigated the ultrastructural distribution of sulfated complex carbohydrates (CC) in the mature cartilage and the perichondrium of young rabbit auricles using the high iron diamine-thiocarbohydrazide-silver proteinate (HID-TCH-SP) and the tannic acid-ferric chloride (TA-Fe) methods. In the mature cartilage, HID-TCH-SP stained intracellular Golgi saccules of the mature face, secretory granules, and the extracellular matrix granules, but staining was not discernible in collagen fibrils and osmiophilic elastic fibers consisting of only amorphous elastin. The HID and TA-Fe staining were similarly observed in matrix granules, whereas the elastic fibers and collagen fibrils lacked the staining. The pericellular matrix granules had a diameter of 34 +/- 5 nm (mean +/- SD; n = 30). Thiéry's periodate-TCH-SP (PA-TCH-SP) method stained vicinal glycol-containing CC in collagen fibrils but failed to stain matrix granules and elastic fibers. In the perichondrium, HID-TCH-SP staining of the organelles was less intense in the flattened chondrocytes when compared with those in large mature chondrocytes. The extracellular HID and HID-TCH-SP staining were observed in the matrix granules. The diameter of pericellular matrix granules (19 +/- 4 nm, mean +/- SD; n = 30) was significantly smaller when compared to those in the mature cartilage (P less than 0.001). The HID-TCH-SP staining was closely associated with collagen fibrils. However, the staining was not seen in collagen fibrils and osmiophilic elastic fibers consisting of elastin and microfibrils. The PA-TCH-SP method stained collagen fibrils and microfibrils but did not stain the amorphous elastin. Thus these studies demonstrate that sulfated CC are packaged in chondrocyte secretory granules and are released into the extracellular matrix to form matrix granules, but are not incorporated into collagen fibrils and elastic fibers.     

大鼠不同部位疏松结缔组织撕片的制备和观察

目的　对比大鼠皮下取材和肠系膜取材制备疏松结缔组织撕片的差异;观察同一部位取材的疏松结缔组织HE染色和醛复红-亮绿-橘黄G染色差异;分析不同部位取材的疏松结缔组织两种染色方法的结果差异。 方法　Wistar大鼠腹腔注射10 g/L苔盼蓝生理盐水溶液2.5 ml,1次/d,连续3 d,分别在皮下、肠系膜取疏松结缔组织,铺片。两个部位的铺片分别采用HE染色、醛复红-亮绿-橘黄G染色。 结果　皮下取材疏松结缔组织经HE染色可见大量成纤维细胞,肥大细胞明显,巨噬细胞可见,弹性纤维和胶原纤维可见,但不明显;皮下取材疏松结缔组织经醛复红-亮绿-橘黄G染色弹性纤维呈紫红色、胶原纤维呈橙色,细胞不易着色;肠系膜取材疏松结缔组织经HE染色,可见成纤维细胞、肥大细胞、巨噬细胞明显,弹性纤维呈蓝紫色、胶原纤维呈淡红色;肠系膜取材疏松结缔组织经醛复红-亮绿-橘黄G染色,弹性纤维被染成紫红色、胶原纤维染成鲜艳的绿色,肥大细胞被染成紫红色,核呈圆或椭圆形、棕黄色,巨噬细胞清晰可见、形态不规则,胞质中可见粗大呈蓝紫色的苔盼蓝颗粒,细胞核呈圆形、棕黄色;成纤维细胞胞质无着色,核呈棕黄色。 结论　大鼠肠系膜取材制备的疏松结缔组织撕片经醛复红-亮绿-橘黄G染色能够更好的显示各种类型细胞和纤维,各结构间对比明显。     

切断大鼠交感神经对动脉粥样硬化形成的影响

将雄性Ｗｉｓｔｒ大鼠１２只分成实验组和对照组，实验组行手术切断左侧颈交感干，两天后与对照组同时腹腔注射维生素Ｄ６０万单位／ｋｇ体重，存活２０天后取双侧颈总动脉作石蜡切片，ＨＥ染色，光镜下观察，结果发现：实验组颈总动脉壁明显增厚，相当于正常血管壁的３－５倍，弹性纤维结构不清，甚至消失，内膜一层水肿并有胶原纤维增生，中膜有大量平滑肌细胞增生，其细胞核排列紊乱。     

Three-dimensional analysis of alveolar structure in usual interstitial pneumonia

The etiology of usual interstitial pneumonia (UIP), a progressive lung disease, remains unclear. We examined alveolar structure in UIP three-dimensionally. Lung biopsy specimens from five patients with idiopathic pulmonary fibrosis were used. Sections 150-microm thick were stained with elastica solution for elastic fibers, with alpha-smooth muscle actin antibody for myofibroblasts, with anti-Thomsen-Friedenreich antibody for type-II pneumocytes and with anti-CD34 antibody for blood vessels. We examined them three-dimensionally using a laser confocal microscope or light microscope. In the fibrotic lesions, the thick elastic fibers forming the alveolar framework were not particularly dense considering the reduction in alveolar volume. Near the fibrotic lesions, some of the thin elastic fibers in the alveolar wall were slightly sinuous and ended with rounded tips. Type-II pneumocytes had proliferated and were distributed uniformly over the alveolar surface. Smooth muscle actin filaments were detected only around the alveolar orifice. These findings show that in UIP destruction of the elastic fiber framework of the alveoli may lead to irreversible focal alveolar collapse after damage to the alveolar epithelial cells, and proliferation of type-II pneumocytes may be involved with this elastolysis.     

Pulmonary elastic fiber degradation in paraquat toxicity. An electron microscopic immunohistochemical study

To study the morphologic alterations of pulmonary elastic fibers in cynomolgus monkeys with paraquat toxicity, peroxidase- and ferritin-labeled antielastin antibodies were used for the light and electron microscopic localization of elastin. One week after paraquat, alveolitis, tissue damage and alveolar dilatation were present; elastic fibers were frayed and more diffusely and intensely stained than those of control animals. In the latter, staining was localized in peripheral regions of the amorphous components and, to a lesser extent, in some microfibrils of elastic fibers. At 3 to 4 weeks, diffuse staining was evident in damaged interstitial elastic fibers and in newly formed elastic fibers in areas of intraalveolar fibrosis. At 8 weeks, the interstitium contained many elastic fibers which showed staining only in peripheral regions of the amorphous components. These observations suggest that: 1) preembedding immunohistochemical staining for elastin is localized in peripheral regions of normal elastic fibers because the antielastin antibody can penetrate into mature and undamaged amorphous components only to a very limited extent; 2) in early stages of paraquat toxicity this staining is more diffuse and intense because elastase from inflammatory cells partially degrades the elastic fibers and permits greater penetration of the antibody into the amorphous materials; 3) in later stages the staining pattern returns to normal as inflammation subsides and elastic fibers are repaired; however, newly formed elastic fibers in areas of intraalveolar fibrosis stain diffusely, reflecting increased penetration of the antibody because of immaturity and incomplete cross-linking, and 4) degeneration of elastic fibers of alveolar walls in paraquat lung may lead to alveolar dilatation, which is associated with irregular fibrosis and constitutes one of the processes of pulmonary structural remodeling in paraquat lung.(ABSTRACT TRUNCATED AT 250 WORDS)     

Light and electron microscopic identification of elastic, elaunin and oxytalan fibers in human tracheal and bronchial mucosa

Summary The elastic fiber system in the human tracheal and bronchial mucosa was studied by light and electron microscopy. Elastic fibers, elaunin fibers, and oxytalan fibers were discerned. These fibers were identified by means of their staining characteristics (elastica stains, methods for disulfide-groups) and on account of their fine structural morphology. Elastic fibers consist of elastin and few elastic-fiber microfibrils. The relative amount of elastin (compared to the amount of elastic-fiber microfibrils) is large in elastic fibers but small in elaunin fibers. Oxytalan fibers — by contrast — are pure bundles of microfibrils.In the light microscope a well-defined elastic lamina separates the lamina propria and the submucosa of the normal mucous membrane. The elastic lamina is formed by coarse strands of longitudinally running elastic fibers. A delicate network of elastica-positive fibers is attached to the basement membrane of the epithelial layer (subepithelial elastic layer). A few of these elastica-positive fibers branch out, traverse the region of the thickened basement membrane, and insert into the basal lamina of the epithelium. A loose network of elastica-positive fibers is present both in the lamina propria and in the submucosa. Plates of cartilage, glandular epithelium, and bundles of smooth muscle cells are enveloped by delicate elastica-positive fibers.Electron microscopy shows the lamina elastica to be predominantly composed of elastic fibers, whilst elaunin fibers from the subepithelial elastic layer. Fibers penetrating the thickened basement membrane of the epithelium are identified as oxytalan fibers. All three types of fibers are present throughout the lamina porpria and in the submucosa. Elaunin fibers and oxytalan fibers comprise the elastica-positive nets around glandular epithelium, smooth muscle bundles, and cartilage. The preferred location of oxytalan fibers (within the thickened basement membrane), elaunin fibers (subepithelial elastica-positive layer), and clastic fibers (lamina elastica) facilitates the comparison of light microscopic staining reactions and fine structural morphology of these fibers.With financial support from the Fonds zur Förderung der Wissenschaftlichen Forschung, project Nr. 4055, and Hochschuljubiläumsstiftung der Stadt Wien. Part of this work has been presented at the 2. Arbeitstagung der Anatomischen Gesellschaft, Würzburg, 8.-10.10.1980     

巨噬细胞在血管重塑过程中的作用

目的:探讨体内巨噬细胞对平滑肌细胞增殖与迁移的影响。方法:采用兔后肢股动脉—静脉短路诱导侧枝血管生长模型。一周后将动物处死,应用Ki67(细胞增殖标记物)免疫荧光组织化学技术和弹性纤维组织化学染色技术,在连续切片上检测髂外动脉在重塑过程中巨噬细胞数目和平滑肌细胞增殖及弹性纤维的降解。结果:在重塑血管外膜发现大量巨噬细胞,中膜也有大量巨噬细胞的存在,平滑肌细胞排列紊乱;有大量的平滑肌细胞增殖。在正常血管横断面上中膜有大量环形排列的弹性纤维存在,重塑的血管巨噬细胞聚集和平滑肌细胞增殖的部位弹性纤维发生明显降解。结论:血管重塑过程中,侵入血管壁的巨噬细胞可能通过分泌生长因子和细胞基质降解酶促进细胞外基质的降解,刺激平滑肌细胞增殖与移动,参与血管重塑的调节。     

Lysyl oxidase is essential for normal development and function of the respiratory system and for the integrity of elastic and collagen fibers in various tissues

Lysyl oxidases, a family comprising LOX and four LOX-like enzymes, catalyze crosslinking of elastin and collagens. Mouse Lox was recently shown to be crucial for development of the cardiovascular system because null mice died perinatally of aortic aneurysms and cardiovascular dysfunction. We show here that Lox is also essential for development of the respiratory system and the integrity of elastic and collagen fibers in the lungs and skin. The lungs of E18.5 Lox(-/-) embryos showed impaired development of the distal and proximal airways. Elastic fibers in E18.5 Lox(-/-) lungs were markedly less intensely stained and more disperse than in the wild type, especially in the mesenchyme surrounding the distal airways, bronchioles, bronchi, and trachea, and were fragmented in pulmonary arterial walls. The organization of individual collagen fibers into tight bundles was likewise abnormal. Similar elastic and collagen fiber abnormalities were seen in the skin. Lysyl oxidase activity in cultured Lox(-/-) skin fibroblasts and aortic smooth muscle cells was reduced by approximately 80%, indicating that Lox is the main isoenzyme in these cells. LOX abnormalities may thus be critical for the pathogenesis of several common diseases, including pulmonary, skin, and cardiovascular disorders.     

Structural relationships between the endothelial actin system and the underlying elastic layer in the distal interlobular artery of the rat kidney

Summary The structure of the intracellular actin filaments and the extracellular matrices was studied in the distal interlobular arteries in the rat kidney, employing three different morphological techniques, including rhodamin-phalloidin staining of cryosections, resorcin-fuchsin staining of paraffin sections, and a cold dehydration procedure for electron microscopy. The endothelial cells possess longitudinally running stress fibers. The inner elastic layer is composed of meshworks of elastic fibers encompassing numerous pores. The smooth muscle cells containing abundant actin filaments are arranged circumferentially around the vascular axis. The endothelial stress fibers are found mainly in the basal half of the endothelial cells, and anchor onto the basal cell membranes. The elastic meshworks send off longitudinal branch fibers to contact the endothelial cell membranes at the anchoring sites of stress fibers. In addition circumferential branches run toward the smooth muscle cells. The functional significance of the intracellular contractile apparatus and the extracellular tensile component in small arteries was discussed.