Viscoelastic properties and collagen content of the long saphenous vein in normal and varicose veins

Psaila, J.V.; Melhuish, J.

doi:10.1002/bjs.1800760112

Cited by 72 publications

(43 citation statements)

References 17 publications

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“…The vein wall dilation would then further distort the valves, leading to further increases in venous pressure and wall dilation. In support of this view, VVs show valve hypertrophy, increased width of the valvular annulus (Corcos et al, 2000), decreased collagen content, and reduced viscoelasticity (Psaila and Melhuish, 1989), as well as increased monocyte and macrophage infiltration and inflammation in the valvular sinuses compared with distal VV walls (Ono et al, 1998). However, venous dilation and VVs are often seen below competent valves (Naoum et al, 2007).…”

Section: Matrix Metalloproteinases In Varicose Veinsmentioning

confidence: 95%

Matrix Metalloproteinases as Regulators of Vein Structure and Function: Implications in Chronic Venous Disease

MacColl

Khalil

2015

J Pharmacol Exp Ther

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Lower-extremity veins have efficient wall structure and function and competent valves that permit upward movement of deoxygenated blood toward the heart against hydrostatic venous pressure. Matrix metalloproteinases (MMPs) play an important role in maintaining vein wall structure and function. MMPs are zinc-binding endopeptidases secreted as inactive pro-MMPs by fibroblasts, vascular smooth muscle (VSM), and leukocytes. ProMMPs are activated by various activators including other MMPs and proteinases. MMPs cause degradation of extracellular matrix (ECM) proteins such as collagen and elastin, and could have additional effects on the endothelium, as well as VSM cell migration, proliferation, Ca 21 signaling, and contraction. Increased lower-extremity hydrostatic venous pressure is thought to induce hypoxia-inducible factors and other MMP inducers/ activators such as extracellular matrix metalloproteinase inducer, prostanoids, chymase, and hormones, leading to increased MMP expression/activity, ECM degradation, VSM relaxation, and venous dilation. Leukocyte infiltration and inflammation of the vein wall cause further increases in MMPs, vein wall dilation, valve degradation, and different clinical stages of chronic venous disease (CVD), including varicose veins (VVs). VVs are characterized by ECM imbalance, incompetent valves, venous reflux, wall dilation, and tortuosity. VVs often show increased MMP levels, but may show no change or decreased levels, depending on the VV region (atrophic regions with little ECM versus hypertrophic regions with abundant ECM) and MMP form (inactive pro-MMP versus active MMP). Management of VVs includes compression stockings, venotonics, and surgical obliteration or removal. Because these approaches do not treat the causes of VVs, alternative methods are being developed. In addition to endogenous tissue inhibitors of MMPs, synthetic MMP inhibitors have been developed, and their effects in the treatment of VVs need to be examined.

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Section: Matrix Metalloproteinases In Varicose Veinsmentioning

confidence: 95%

Matrix Metalloproteinases as Regulators of Vein Structure and Function: Implications in Chronic Venous Disease

MacColl

Khalil

2015

J Pharmacol Exp Ther

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“…Heredity is an important factor as more than half of those affected have a positive family history, suggesting a congenital weakness of the vein wall (Travers et al, 1996). The weak wall theory with secondary valvular incompetence has been proposed as the most likely cause of primary varicose veins (Psaila & Melhuish, 1989). Primary wall weakness explains why varicosities are often found below competent valves (Rose and Ahmed, 1986).…”

Section: Introductionmentioning

confidence: 99%

Smooth Muscle Changes in Varicose Veins: An Ultrastructural Study

Wali

Eid

2001

J. Smooth Muscle Res.

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In order to understand the pathology of varicose veins, we prospectively collected a total of 23 vein specimens both from the normal proximal thigh long saphenous vein (LSV) in 3 young trauma patients and from the unstripped proximal LSV near the sapheno-femoral junction and the distal calf blowouts in 10 primary varicose veins patients. Ultra-thin sections were examined under the transmission electron microscope (TEM). Compared with the normal control LSV, varicose vein sections showed increase in the diameter of the lumen, hypertrophy of the wall and elongation and invagination of the intima. Smooth muscle cells (SMCS) lost their normal fusiform shape and were widely separated by increased amounts of extra-cellular collagen fibers. The cells underwent marked degeneration, vacuolization and disintegration into fiber-like material and small separated fragments. SMCs were seen in the subintimal tissue and some of them were lost into tile lumen. SMCs also showed marked phagocytic activity, engulfing not only collagen and elastic fibers, but also other smooth muscle cells. Although these changes were more marked and advanced in the distal calf blowouts, they were also present in the proximal, clinically non-dilated LSV. In conclusion, SMCs of varicose veins show severe degeneration in both the distal calf blowouts and the proximal, clinically non-varicose LSV. It appears that they both form and phagocytose collagen and elastic fibers and play a major role in the pathogenesis of varicose veins.

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“…The exact etiology of this disease remains unknown. Although valvular incompetence has long been held as the primary cause of varicose veins, dilatation of the veins precedes the valvular dysfunction [1, 2, 3]. This may indicate that the primary defect leading to varicose veins resides in a dysfunction of the venous wall [4].…”

Section: Introductionmentioning

confidence: 99%

Imbalance in the Synthesis of Collagen Type I and Collagen Type III in Smooth Muscle Cells Derived from Human Varicose Veins

et al. 2001

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Varicose veins have a thickening wall. Their smooth muscle cells are disorganized as regards proliferation and production of extracellular matrix protein. An imbalance between the synthesis of collagen type I protein (collagen I) and collagen type III protein (collagen III) could explain the lack of elasticity of varicose veins. Therefore, collagen synthesis was compared in the media and in cultured smooth muscle cells derived from human control and varicose saphenous veins. An increase in total collagen synthesis was observed in the media and in smooth muscle cells derived from varicose veins. This augmentation was due to an overproduction of collagen I in cultured cells from varicose veins consistent with an increase in the release of collagen I metabolites in the media. A concomitant decrease in collagen III was observed in cultures of smooth muscle cells from varicose veins. The increase in the synthesis of collagen I in cells from varicose veins was correlated with an overexpression of the gene since mRNAs for collagen I were augmented without change in mRNA-half-life. This augmentation in the synthesis of collagen I was reduced by the addition of exogenous collagen III in cultures from varicose veins. These findings suggest a dysregulation of the synthesis of collagen I and III in smooth muscle cells derived from varicose veins.

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Viscoelastic properties and collagen content of the long saphenous vein in normal and varicose veins

Cited by 72 publications

References 17 publications

Matrix Metalloproteinases as Regulators of Vein Structure and Function: Implications in Chronic Venous Disease

Matrix Metalloproteinases as Regulators of Vein Structure and Function: Implications in Chronic Venous Disease

Smooth Muscle Changes in Varicose Veins: An Ultrastructural Study

Imbalance in the Synthesis of Collagen Type I and Collagen Type III in Smooth Muscle Cells Derived from Human Varicose Veins

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