elastin has been researched along with Varicose-Veins* in 26 studies
1 review(s) available for elastin and Varicose-Veins
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Extracellular matrix remodeling in the vascular wall.
The extracellular matrix provides a structural framework essential for the functional properties of vessel walls. The three dimensional organization of the extracellular matrix molecules--elastin, collagens, proteoglycans and structural glycoproteins--synthesized during fetal development--is optimal for these functions. Early in life, the vessel wall is subjected to injury: lipid deposition, hypoxia, enzyme secretion and reactive oxygen species production during inflammatory processes, and the extracellular matrix molecules are hydrolyzed by proteases--matrix metalloproteinases, leukocyte elastase, etc. In uninjured arteries and veins, some proteases are constitutively expressed, but through the control of their activation and/or their inhibition by inhibitors, these proteases have a very low activity. During the occurrence of vascular pathologies--atherosclerosis, hypertension, varicosis, restenosis, etc.--the balance between proteases and their inhibitors is temporally destroyed through the induction of matrix metalloproteinase gene expression or the secretion of enzymes by inflammatory cells. Smooth muscle cells, the most numerous cells in vascular walls, have a high ability to respond to injury through their ability to synthesize extracellular matrix molecules and protease inhibitors. However, the three dimensional organization of the newly synthesized extracellular matrix is never functionally optimal. In some other pathologies--aneurysm--the injury overcomes the responsive capacity of smooth muscle cells and the quantity of extracellular matrix decreases. In conclusion, care should be taken to maintain the vascular extracellular matrix reserve and any therapeutic manipulation of the protease/inhibitor balance must be perfectly controlled, because an accumulation of abnormal extracellular matrix may have unforeseen adverse effects. Topics: Aneurysm; Animals; Blood Vessels; Collagen; Coronary Disease; Elastin; Extracellular Matrix; Extracellular Matrix Proteins; Humans; Hypertension; Varicose Veins | 2001 |
1 trial(s) available for elastin and Varicose-Veins
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Assessment of wall structure and composition of varicose veins with reference to collagen, elastin and smooth muscle content.
To compare collagen, elastin and smooth muscle contents of varicose and control long saphenous veins.. Collagen, elastin and muscle were estimated stereologically using random sampling and histological staining.. Varicose vein samples were collected from nine patients (mean age 52 years, range 34-64 years) undergoing vein stripping, sample sites being saphenofemoral junction and knee. Control samples were taken from five patients (mean age 58 years, range 38-76 years) presenting for femoral-popliteal bypass at equivalent levels.. Veins were fixed, sectioned transversely, and stained with Picric Acid Sirius Red. Analysis of samples was performed using point and intersection counting on vertically projected images.. Using two way analysis of variance tests, varicose saphenous veins had significantly larger wall areas (p < 0.01) and higher amounts of collagen (p < 0.01). Collagen content and wall area were significantly larger proximally compared to distally in both control and varicose veins (p < 0.05) with a higher content of smooth muscle and elastin in varicose veins proximally compared to distally (p < 0.05). There was no difference in wall thickness or elastin content between the two groups.. This suggests that varicose veins are a dynamic response to venous hypertension and are not thin walled structures as previously thought. Topics: Adult; Aged; Analysis of Variance; Collagen; Elastin; Histocytochemistry; Humans; Middle Aged; Muscle, Smooth, Vascular; Saphenous Vein; Staining and Labeling; Varicose Veins | 1996 |
24 other study(ies) available for elastin and Varicose-Veins
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Expression levels of elastin and related genes in human varicose veins.
Among the suspected reasons for varicose vein formation are changes in the quantity and content of the elastin protein; however, comprehensive investigations about elastin assembly in varicose vein formation are yet lacking. In this study, we aimed to determine the changes in mRNA levels of elastin and some of its functionally related proteins, fibulin 5, LOXL-1, MMP-2 and MMP-9 in varicose vein formation. We analysed the mRNA levels of elastin, fibulin-5, LOXL1, MMP2 and MMP9 in samples of 35 healthy and 35 varicose great saphenous vein tissues. mRNA levels of these genes were determined by using real-time PCR and normalized with HPRT1. When we compared the patient and control groups, elastin mRNA levels were significantly higher in the patient group than in the control group (P = 0.047), although there were no significant differences in fibulin 5, LOXL1, MMP2 and MMP9 mRNA levels between the patient and control groups. We showed that up-regulation of MMP2 mRNA expression was significantly correlated with hyperlipidaemia (P = 0.029). The up-regulation of elastin expression may play an important role in the pathogenesis of primary varicose veins. Additionally, the up-regulation of MMP2 expression was strongly correlated with hyperlipidaemia in varicose veins. Topics: Aged; Amino Acid Oxidoreductases; Elastin; Extracellular Matrix Proteins; Female; Humans; In Vitro Techniques; Male; Matrix Metalloproteinase 2; Middle Aged; Varicose Veins | 2014 |
Valve disease in chronic venous disorders: a quantitative ultrastructural analysis by transmission electron microscopy and stereology.
The ultrastructure of venous valves and walls in chronic venous disease was investigated.. Consecutive patients were categorised into one of three groups (group A: patients with C1 venous disease in accordance with CEAP (Clinical severity, Etiology, Anatomy, Pathophysiology); group B: C2 and C3; group C: C4, C5 and C6). The terminal or preterminal valve and adjacent vessel wall was harvested from the great saphenous vein. Sections were examined with a transmission electron microscope. The volumes of elastin and of collagen per unit surface area of valve were assessed, as well as the surface endothelium of valve and vessel wall.. The study population consisted of 17 patients. The elastin ratio was analysed by means of stereology. Mean values were: in group A, 0.45 μm3/m2; in group B, 0.67 μm3/m2; in group C, 0.97 μm3/m2. The ratio was similar for collagen (A, 15.7 μm3/m2; B, 26.8 μm3/m2; C, 30.1 μm3/m2). Surface analysis of the valve endothelium and the adjacent vessel wall endothelium showed a trend towards increasing damage with more severe disease.. With progression of venous disease, the valve elastin content, assessed morphologically, seems to increase, and the endothelium of the venous valve and the vein wall tend to show more damage. Topics: Adult; Aged; Biomarkers; Chronic Disease; Collagen; Disease Progression; Elastin; Endothelium, Vascular; Female; Humans; Male; Microscopy, Electron, Transmission; Middle Aged; Saphenous Vein; Single-Blind Method; Varicose Veins; Venous Valves | 2013 |
Selective loss of extracellular matrix proteins is linked to biophysical properties of varicose veins assessed by ultrasonography.
Dilatation and enhanced distensibility are specific biophysical properties of varicose veins. Both can be assessed by ultrasonography. The aim of this study was to analyse correlations between the vein wall protein content and these two biophysical properties of varicose veins.. Twenty-seven patients having surgery for varicose veins and six control patients with normal veins undergoing arterial bypass surgery were examined clinically and with ultrasonography the day before surgery. Fifty-two varicose and six control vein rings were harvested and analysed histopathologically and morphometrically; vascular tissue microarrays incorporated 116 vein wall sectors.. Elastin loss in the adventitia (P = 0.010) and reduction of type III collagen in the intima and media (P = 0.004) were observed in varicose veins. Elastin loss correlated negatively with vein diameter at rest (P = 0.005), whereas loss of type III collagen in the intima correlated negatively with the increase in vein diameter at the Valsalva manoeuvre (P < 0.001).. Loss of elastin and type III collagen occurs in varicose veins and can be assessed with ultrasonography in vivo by measuring vein diameter and distensibility. Topics: Adult; Case-Control Studies; Collagen Type III; Elastin; Extracellular Matrix Proteins; Female; Humans; Immunohistochemistry; Male; Microarray Analysis; Middle Aged; Prospective Studies; Saphenous Vein; Ultrasonography; Varicose Veins | 2007 |
Role of saphenous vein wall in the pathogenesis of primary varicose veins.
Varicose veins may be due to weakness of the vein wall as a result of structural problems. There are conflicting findings in the literature about these problems especially concerning collagen, elastin and smooth muscle cells content. The aim of this study was to look at the structural abnormalities of varicose veins (with and without valvular incompetence).. We studied 70 specimens of long saphenous veins from 35 patients (24 with varicose and 11 with normal veins). Two specimens were taken from each vein approximately 3-4 cm from the saphenofemoral junction. Vein specimens were processed for histological and electron microscopic studies. Both qualitative and quantitative analyses were performed to assess the degree of wall changes. Using the image analyzer, contents of collagen, elastin and smooth muscle cells, in addition to intimal and medial thickness, were measured.. Light microscopy revealed significant increase in intimal and medial thickness and collagen content of media and significant decrease in elastin content in varicose veins compared with normal veins. There was no statistical significant difference between varicose veins with and without saphenofemoral valve incompetence. Electron microscopy showed marked degenerative changes in intima and media of varicose veins.. The findings in our study supported the theory of primary weakness of the vein wall as a cause of varicosity. This weakness is due to intimal changes, disturbance in the connective tissue components and smooth muscle cells. Topics: Adult; Case-Control Studies; Collagen; Egypt; Elasticity; Elastin; Female; Humans; Male; Microscopy, Electron; Myocytes, Smooth Muscle; Saphenous Vein; Saudi Arabia; Staining and Labeling; Tunica Intima; Tunica Media; Varicose Veins; Venous Insufficiency | 2007 |
ICVTS on-line discussion A. Valves and primary varicose veins.
Topics: Collagen; Elasticity; Elastin; Humans; Microscopy, Electron; Myocytes, Smooth Muscle; Saphenous Vein; Staining and Labeling; Tunica Intima; Tunica Media; Varicose Veins; Venous Insufficiency | 2007 |
A journey across the wall of varicose veins: what physicians do not often see with the naked eye.
To examine varicose veins (VVs) from inside out in order to help surgeons and general practitioners better understand the pathogenesis of the disease and improve their management.. A comprehensive examination of the wall of VVs was performed using transmission electron microscopy. The ultrastructural morphology of the collagen, elastin and smooth muscle content of the wall was analyzed in a sample of 10 patients (4 male and 6 female) and 10 matched controls aged between 37 and 50 years.. Analysis of the tunica media revealed that the smooth muscle cells were significantly separated from each other by a marked increase in amorphous and fibrous tissue in which many of the collagen and elastin fibers lost their normal structural arrangement. The cells contained a large number of membrane-bound intracellular vesicles and cytoplasmic vacuoles. The collagen fibers were smaller and thinner than what is commonly seen in normal veins, and they were widely separated from each other. A light electron-lucent center was observed in the middle of the fibers. Similar changes were also seen in the intima and were associated with irregular plaque-like intimal thickening.. Our study revealed a significant separation among smooth muscle cells in the wall of VVs, and the presence of an abnormal amorphous extracellular matrix and intracytoplasmic vacuoles could reflect 'unusual' possible secretory and phagocytic roles of smooth muscle cells. This could provide an important explanation for the abnormal contractile function of these cells in VVs. Topics: Adult; Case-Control Studies; Collagen; Elastin; Female; Health Knowledge, Attitudes, Practice; Humans; Male; Microscopy, Electron, Transmission; Middle Aged; Muscle, Smooth, Vascular; Physicians; Saudi Arabia; Varicose Veins | 2006 |
Identification of differentially expressed genes in primary varicose veins.
A number of changes in protein expression have been described in primary varicose veins, but the altered gene expressions in this disease are unknown. The aim of this study was to identify differentially expressed genes in primary varicose veins.. Total RNAs were isolated from two groups of greater saphenous veins (four primary varicose veins and three normal) and then were reverse transcribed into cDNAs. We used the differential display reverse transcription-polymerase chain reaction technique to screen the differences in the mRNA expression profiles of the groups.. We found that three cDNAs showed differences in expression patterns between normal and diseased saphenous veins. The cDNAs are prominently expressed only in patients with varicose veins. We identified that the cDNAs had significant similarities to the L1M4 repeat sequence of clone RP11-57L9, clone RP11-299H13, and Alu repetitive sequence of human tropomyosin 4 mRNA.. Our results suggest that the screened cDNA clones are useful disease markers in the genetic diagnosis of primary varicose vein and that the L1 and Alu elements possibly participated in the development of primary varicose veins through their expression patterns in genes encoded with structural proteins, such as collagen, elastin, and tropomyosin. Further studies are required to elucidate the potential relationship between repeat sequences and primary varicose veins. Topics: Collagen; DNA, Complementary; Elastin; Gene Expression Profiling; Humans; Tropomyosin; Varicose Veins; Veins | 2005 |
Smooth muscle cell apoptosis in primary varicose veins.
One of the important factors responsible for vessel wall remodelling is programmed cell death. In the paper the role of smooth muscle cell (SMC) apoptosis in primary varicose veins (PVV) is investigated.. Vein specimens were obtained from 40 patients with PVV. In each case proximal and distal (upper crural) great saphenous veins (GSV) were harvested. Morphometric computer assessed quantitative evaluation of SMCs, collagen and elastin content was carried out. Apoptotic cells were detected by TUNEL assay. The levels of p53, BAX, BCLl-2 and p21 mRNA expression were assessed by real time RT-QPCR and the presence of respective proteins in the vessel wall was confirmed by immunohistochemistry.. In the proximal GSV segments a significant increase of p53, p21 and BCL-2 mRNA levels was found in PVV patients. In the distal segments BAX and BCL-2 expression levels were higher. Taking into account the patient age, elevated p53 mRNA expression level was noticed in the distal incompetent GSVs of young PVV patients. In this group a statistically significant increase in the apoptotic index (APIx) within the vein media was found which correlated positively with p53 mRNA expression level. There was no increase of the apoptotic activity in elderly patients that led to the structural changes increase. In proximal GSV segments, despite SMC amount reduction or presence of structural changes in perivalvular wall region, no increase of the APIx with was noticed.. P53-related apoptosis is one of the regulatory mechanisms of vein wall homeostasis maintenance. During varicose vein development its activation is related to the early stages of the disease. In the further course, the down-regulation of the SMC apoptosis within the vein media leads to the structural changes increase. The reduction of the SMC population corresponding to an increase of p21 expression in proximal saphenous vein segments suggests that the cell cycle disturbances may lead to the 'weakness' of the proximal GSV wall. Valve injury is not the only factor leading to the varicose veins occurrence. Topics: Adult; Apoptosis; bcl-2-Associated X Protein; Collagen; Elastin; Female; Gene Expression; Humans; Immunohistochemistry; Male; Middle Aged; Muscle, Smooth, Vascular; Proto-Oncogene Proteins c-bcl-2; Tumor Suppressor Protein p53; Tunica Intima; Varicose Veins | 2004 |
Expression of elastic components in healthy and varicose veins.
This study evaluates possible changes in the synthesis/degradation of elastic components of the vein wall in an attempt to explain the development of varicosis. Healthy and varicose saphenous veins were subjected to immunohistochemical analysis using anti-elastin, anti-fibrillin-1, anti-elastase, anti-transforming growth factor (TGF)-beta and anti-latent TGFbeta binding protein (LTBP)-2 monoclonal antibodies. In situ hybridization was performed using specific probes for tropoelastin and fibrillin-1. In healthy veins, elastin and fibrillin-1 showed even, overlapping distribution patterns indicating their particular abundance in the adventitia and at the intima/media interface. The expression of tropoelastin and fibrillin-1 was high in smooth muscle cells bordering the elastic laminae. Elastin, fibrillin-1, and cells expressing fibrillin-1 and tropoelastin mRNA showed a patchy disorganized pattern, particularly in the proximal varicose segments of patients under 50 years of age. Enhanced elastase activity was noted in both control and varicose specimens from elderly subjects. Varicose veins specimens showed greater LTBP-2 and TGF expression. Both molecules were detected in the subendothelium and the media, particularly in areas of marked injury. Our findings suggest that the development of the varicose condition involves a restructuring of the elastic component of the vein wall, perhaps as a consequence of changes in the transcription mechanisms of muscle layer cells. Topics: Adaptor Proteins, Signal Transducing; Adult; Aged; Carrier Proteins; Elastin; Extracellular Matrix; Humans; Immunohistochemistry; In Situ Hybridization; Latent TGF-beta Binding Proteins; Middle Aged; Muscle, Smooth, Vascular; Saphenous Vein; Transforming Growth Factor beta; Varicose Veins | 2003 |
Changes of elastic and collagen fibers in varicose veins.
The resistance to stretch and the elasticity of the vein wall depend on the collagen and elastic fibers, respectively. Contradicting evidence exists, however, on the connective tissue concentration in varicose veins.. A prospective, comparative study was conducted at Asir Central Hospital and the College of Medicine in Abha, Saudi Arabia. Twenty-three vein specimens collected from both the proximal thigh long saphenous vein (LSV) and the distal calf blowouts in 10 primary varicose vein patients and from the normal, proximal thigh LSV in 3 young vascular trauma patients were examined. Paraffin sections stained with hematoxylin and eosin, Verhoeff von Gieson (VVG) and Masson's Trichrome stains were examined under the light microscope. Ultra thin sections were examined under the transmission electron microscope (TEM).. Compared with the normal control LSV, varicose vein sections showed increased diameter of the lumen and hypertrophy of the wall, mainly of the intima, due to increased amounts of collagen fibers. This marked fibrous infiltration disrupted the normal palisade arrangement of the intimal and the regular sheet-like arrangement of the medial smooth muscle cells. Collagen fibers also lost their normal pattern and showed abnormal forms. Elastic fibers lost their regular laminar arrangement and formed clumps or scattered fragments.. Varicose veins showed increased collagenosis and distortion of the elastic fibers. The presence of abnormal collagen to elastin ratio and the loss of the regular collagen/elastic lattice of the vein wall may play a major role in the pathogenesis of varicose veins. Topics: Adolescent; Adult; Collagen; Elasticity; Elastin; Endothelium, Vascular; Female; Humans; Male; Middle Aged; Myocytes, Smooth Muscle; Prospective Studies; Saphenous Vein; Varicose Veins | 2002 |
Structural changes in the tunica intima of varicose veins: a histopathological and ultrastructural study.
Many factors have been implicated in the aetiology of varicose veins; however, there is ample evidence implicating that the defect is in the wall of the lower limb veins. In order to know the pathological changes in the tunica intima of varicose veins, the smooth muscle cells (SMCs), collagen and elastin of varicose and control patients were studied by light and electron microscopy. The morphological changes in the SMCs, collagen and elastin point to a possible secretory or phagocytic role of the SMCs in producing abnormal immature collagen or elastin fibres or in modulation of function of SMCs due to excessive production of extracellular matrix (ECM). Topics: Adult; Collagen; Elastin; Endothelium, Vascular; Female; Humans; Male; Microscopy, Electron; Middle Aged; Muscle, Smooth, Vascular; Saphenous Vein; Tunica Intima; Varicose Veins | 2000 |
The determination of the collagen and elastin amount in the human varicose vein by the computer morphometric method.
The results of the works dealing with alterations of the connective tissue in varicose vein wall are not ambiguous, so the exact cause of the vein dilatation has still not been established. We were determining the collagen and elastin amounts in human varicose vein wall in comparison with non-dilated long saphenous vein by the light microscopy and computer morphometric method. We have found the lesser amount of collagen in varicose veins than in non-dilated veins, the amounts of the elastin in both the varicose and non-varicose veins were without the statistical significance. Topics: Case-Control Studies; Collagen; Computers; Elastin; Humans; Methods; Saphenous Vein; Varicose Veins | 1999 |
Vascular remodeling in varicose veins.
The present study describes the histopathologic aspects of varicose (n=29; mean age, 52 +/- 12 years) and normal saphenous veins (n=17; mean age, 51 +/- 12 years) of patients from a similar age group. We focused on the changes that occur in the circular layer of the venous wall. We examined the venous walls by light microscopy and transmission electronmicroscopy. A semiquantitative grading system was used to assess the smooth muscle cell (SMC) hypertrophy and the change that occurs in the elastin pattern. The volume densities (Vv) of SMC and collagen were measured as well as the diameter of the SMC, and the nuclei of SMC per fixed area were counted. The varicose vein wall differed from the normal saphenous vein by the presence of hypertrophic SMC as well as disorganized elastin patterns. A correlation between the hypertrophic SMC and an abnormal elastin pattern was observed (r=0.658, p<0.001). Ultrastructurally, the SMC show prominent microherniations and vesicles that bud from the cell. These vesicles contain microfilaments and microtubuli, although no other organelles could be detected. The elastin fibers are disrupted from the hypertrophic SMC. No significant difference could be detected in both the Vv of SMC and the Vv of collagen. The diameter of the SMC in the varicose vein (d=9.45 +/- 1.22 microm) differs significantly from that in the normal saphenous vein (d=6.22 +/- 1.47 microm) (p<0.001). Also, the nuclei of SMC per fixed area differs significantly between the varicose (87 +/- 18) and nonvaricose (117 +/- 24) veins (p<0.001). We conclude that the cellular hypertrophy of the SMC and the microherniations could be the basis for disruption of the elastin fibers connected to the SMC in varicose veins. Disrupted connections between SMC and elastin fibers could in turn induce the weakness of the venous wall observed in varicose vein disease. Topics: Adult; Elastin; Humans; Middle Aged; Muscle, Smooth; Saphenous Vein; Varicose Veins | 1998 |
Biochemical assay of collagen and elastin in the normal and varicose vein wall.
Alterations of the connective tissue in the varicose vein wall have been noted by several investigators; however, the cause of the vein dilatation has still not been established. The aim of this study was to find a biochemical explanation to the development of varices by evaluating sensitive biochemical markers of collagen and elastin in the varicose vein wall. 4-L-Hydroxyproline (HYP), as a marker of collagen content, and desmosine (DES) and isodesmosine (IDES), as markers of elastin, were measured in 47 macroscopically dilated and 32 nondilated segments of 20 varicose saphenous veins collected from 20 patients with varices. The same measurements were made in 24 fragments of normal saphenous veins collected from 14 patients in whom the vein was removed to be used for graft procedures. HYP (collagen) and DES and IDES (elastin) were determined with a colorimetric method and HPLC, respectively. ANOVA test was used to compare mean values (+/- SD). HYP and collagen content were similar in varicose and normal veins. There was a significant reduction of both DES and IDES in dilated segments of varicose veins (P < 0.05 vs normal veins and nondilated segments); the ratio of elastin to collagen was lower in varicose than normal veins (P < 0.05), and this reduction was most significant in the dilated segments (P < 0.01 vs normal veins). These results suggest that dilatation of the varicose vein wall may be related to some defect of elastin metabolism. Further studies on the metabolic activity of vein muscle cells are required. Topics: Adult; Aged; Biochemistry; Collagen; Desmosine; Elastin; Female; Humans; Hydroxyproline; Isodesmosine; Male; Middle Aged; Muscle, Smooth, Vascular; Reference Values; Ultrasonography, Doppler, Color; Varicose Veins; Veins | 1996 |
Analysis of collagen and elastin content in primary varicose veins.
Topics: Collagen; Elastin; Humans; Saphenous Vein; Varicose Veins | 1994 |
Analysis of the connective tissue matrix and proteolytic activity of primary varicose veins.
Valvular incompetence and venous wall abnormalities have been suggested as primary etiologic factors responsible for the development of varicose veins. This study was conducted to evaluate the connective tissue constituents of greater saphenous varicosities. Proteolytic activity, a factor that can lead to matrix degradation and cause weakening and dilation of the venous wall, was also assessed.. The collagen and elastin contents of 16 nonthrombophlebitic greater saphenous varicose veins (VV) and seven normal greater saphenous veins (NV) were quantified. In addition, four duplex scanning-confirmed competent segments of greater saphenous veins (i.e., potential varicose veins [PV]) affected by varicosis at alternate sites were analyzed. Proteolytic activity was determined by zymography and radiolabeled substrate assay.. The content of collagen was significantly increased in the VV and PV compared with NV (VV = 189 +/- 7 mg/gm, PV = 189 +/- 9 mg/gm vs NV = 144 +/- 10 mg/gm, p < 0.05). Conversely, the elastin content in the VV and PV was significantly reduced (VV = 53 +/- 3 mg/gm, PV = 50 +/- 4 mg/gm vs NV = 74 +/- 4 mg/gm, p < 0.05). The collagen to elastin ratio demonstrated an alteration in VV and PV compared with NV (VV = 3.7 +/- 0.3, PV = 3.9 +/- 0.4 vs NV = 2.0 +/- 0.2, p < 0.05). Casein and gelatin zymography did not demonstrate significant qualitative differences in the enzymatic activities among the three groups. Quantitative analysis of the elastase activity in the venous tissues was similarly not appreciably altered (VV = 5.1 +/- 0.2 U/gm, PV = 5.3 +/- 0.2 U/gm vs NV = 5.7 +/- 0.3 U/gm).. A significant increase in the collagen content and a significant reduction in the elastin content of VV were demonstrated. The net increase in the collagen/elastin ratio is indicative of an imbalance in the connective tissue matrix. The biochemical profile of PV was similar to VV and significantly different from NV. These preliminary data support the presence of connective tissue abnormalities before valvular insufficiency. In addition, the absence of an increase in the proteolytic activity excludes enzymatic matrix degradation as an essential component in the formation of venous varicosities. Topics: Collagen; Connective Tissue; Elastin; Female; Gelatinases; Humans; In Vitro Techniques; Male; Metalloendopeptidases; Middle Aged; Pancreatic Elastase; Peptide Hydrolases; Saphenous Vein; Varicose Veins | 1993 |
Histomorphological and pathobiochemical changes of varicose veins. A possible explanation of the development of varicosis.
The authors should like to contribute to the unsettled problem of the development of varicose venous disease with their own experience. They evaluate parallel the histomorphological observations and certain pathobiochemical changes which can be recognized in exstirpated varicose veins. Fourty five stripped saphenas have been studied. They were divided into two groups: a macroscopically normal and a varicose one. The varicose patients were divided again into two subsamples according to the occurrence or lack of thrombophlebitis in their medical case history. The authors were looking for the appropriate pathobiochemical changes of the vessel walls running parallel to the usual histopathological changes. It seems quite possible that the effect which triggers the development of the disease could be anything which causes hypoxia, alters the energy metabolism of the otherwise bradytrophic vascular tissues. Accumulation of proteoglycans, as well as collagen and elastic fibers in place of the smooth muscle cells may cause a decrease in the elasticity of the veins and may produce favourable conditions to thrombus formation and local inflammation. Topics: Carbon Dioxide; Collagen; Elastin; Electron Transport Complex IV; Female; Humans; Lactates; Lactic Acid; Male; Middle Aged; Proteoglycans; Saphenous Vein; Thrombophlebitis; Thromboxane A2; Tissue Plasminogen Activator; Varicose Veins | 1990 |
Biochemical analysis of dermal connective tissue in subjects affected by primary uncomplicated varicose veins.
Biochemical analysis of dermal connective tissue was carried out in 14 subjects affected by primary uncomplicated varicose veins and 14 controls. Skin samples were taken, according to fixed criteria, from operation pieces of total mastectomy for breast cancer. The results suggest that the dermal tissue in these subjects is just thinner than that of controls, confirming previous similar clinical findings. The elective reduction of the collagen content observed, unassociated with changes of other components of the dermal connective tissue, brings evidence for a systemic biochemical defect of the extracellular matrix i.e. a collagen defect affecting the entire body structure and not only the varicose or pre-varicose veins of the lower limbs. Topics: Adult; Aged; Carbohydrates; Collagen; Connective Tissue; Elastin; Female; Glycoproteins; Humans; Leg; Middle Aged; Proteins; Skin; Varicose Veins | 1985 |
[Individual variability in the structure of the walls of the principal trunks of the subcutaneous veins of the lower extremities of the human fetus].
Certain regional peculiarities are noted in the development process of the human principle trunks of the subcutaneous veins during antenatal period. In the fetuses of all ages the wall thickness of the subcutaneous veins is the greatest in the femur, and the middle tunic is better developed in the shin. The vein structure depends on the type of architectonics: at the magistral type (86%) the walls in the large and minor subcutaneous veins are thick with well developed smooth myocytes and connective tissue fibers; at the reticulate type (14%) the walls are thin, their elements are poorly developed. When there is mentioned varicosity of the lower extremity veins in the parents' anamnesis, in fetuses (57%) all the tunics in the venous wall develop more poorly, there is retardation in formation of smooth myocytes and in maturation of collagen fibers. This results in less amount of contractile structures in the middle tunic and optic density of collagen is less manifected. Topics: Collagen; Elastin; Humans; Leg; Muscle, Smooth, Vascular; Varicose Veins; Veins | 1985 |
Connective tissue in varicose veins.
The collagen, elastin, total sugar, and nonscleroprotein content was evaluated in 32 samples of saphenous varicose vein and in 34 controls. A significantly lower collagen and elastin content was found in the varicose samples without correlation with the degree of pathologic broadening. Otherwise the total sugars and the soluble nonscleroproteins were found to be increased in varicose samples. The results are more significant when expressed as milligrams per surface unit of endothelium. Our data support the hypothesis that the decrease in collagen and elastin content is a primary rather than secondary change. Topics: Carbohydrates; Collagen; Connective Tissue; Elastin; Humans; Proteins; Saphenous Vein; Varicose Veins | 1979 |
[Experimental bases for the pharmacology of flavonoids].
Topics: Animals; Arteries; Cattle; Collagen; Elasticity; Elastin; Flavonoids; Glucose; Glycosaminoglycans; Humans; Lactates; Lysosomes; Muscle Contraction; Muscles; Varicose Veins; Veins | 1972 |
[Epidemiology of leg ulcer, a remark on its etiology].
Topics: Adolescent; Adult; Age Factors; Aging; Child; Child, Preschool; Collagen; Elastin; Female; Humans; Infant; Infant, Newborn; Leg Ulcer; Male; Middle Aged; Netherlands; Occupations; Sex Factors; Varicose Veins | 1970 |
BIOCHEMICAL DIFFERENCES IN THE COMPOSITION OF PRIMARY VARICOSE VEINS.
Topics: Cadaver; Collagen; Elastin; Histocytochemistry; Humans; Muscles; Proteins; Varicose Veins; Vascular Surgical Procedures | 1964 |
Content of collagen, elastin, and hexosamine in primary varicose veins.
Topics: Collagen; Elastic Tissue; Elastin; Hexosamines; Humans; Varicose Veins | 1963 |