Plasma elastase in venous disease

Shields, D. A.; Andaz, Shahriyour; Sarin, S.; Scurr, J. H.; Smith, Philip

doi:10.1002/bjs.1800811033

Cited by 69 publications

(31 citation statements)

References 30 publications

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“…In our earlier work [35, 36, 37, 38, 39, 40, 41], we found evidence of leucocyte activation and raised levels of endothelial adhesion molecules. The most likely explanation for these observations is that venous disease is associated with a systemic inflammatory response and a pro-inflammatory state of the endothelium.…”

Section: Implications For Pharmacological Treatment In Venous Diseasesupporting

confidence: 53%

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Neutrophil Activation and Mediators of Inflammation in Chronic Venous Insufficiency

Smith¹

1999

J Vasc Res

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The effect of venous hypertension on the state of activation of leucocytes has been investigated in patients with venous disease and control subjects. Leucocytes become ‘trapped’ in the circulation of the leg during periods of venous hypertension produced by sitting or standing. This is greater in the limbs of patients with chronic venous disease than controls. Studies of the plasma levels of neutrophil granule enzymes show that these are increased during periods of venous hypertension, suggesting that this causes activation of the neutrophils. Investigation of the leucocyte surface ligand CD11b shows that the more activated neutrophils and monocytes are sequestered during venous hypertension. Measurement of plasma levels of the soluble parts of the vascular (VCAM), intercellular (ICAM) and endothelial leucocyte (ELAM) adhesion molecules show that these are all elevated in patients with chronic venous disease compared to controls. Following 30 min of venous hypertension produced by standing, these levels are further increased. These data suggest that venous hypertension causes neutrophil and monocyte activation, which in turn causes injury to the endothelium. I believe that this may be the mechanism that initiates the pathological processes which lead to venous ulceration. It has recently been shown that the venotonic drug Daflon 500 mg (450 mg diosmin, 50 mg hesperidin, Servier, France) influences these processes. Surface expression of CD62L is reduced in neutrophils and monocytes, and plasma levels of soluble endothelial adhesion molecules are reduced. These observations may explain the anti-inflammatory effects of Daflon 500 mg.

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Section: Implications For Pharmacological Treatment In Venous Diseasesupporting

confidence: 53%

“…Blood was taken from the arm veins of patients (not the lower limb veins) of patients with varicose veins, liposclerotic skin change and active venous ulceration [39, 40]. In each group, the median level of lactoferrin and elastase was higher in the patients than in the age- and sex-matched controls (fig.…”

Section: Leucocyte Activationmentioning

confidence: 99%

Neutrophil Activation and Mediators of Inflammation in Chronic Venous Insufficiency

Smith¹

1999

J Vasc Res

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“…There is no mention in the literature of these PMN parameters in this clinical condition. It is believed that the behavior of the cytosolic Ca 2+ concentration of PMN cells in these patients might express the basal activation of granulocytes [26][27][28][29], although confirmation comes from studies evaluating the plasma elastase [8] and lactoferrin levels [7] observed in this clinical condition.…”

Section: Discussionmentioning

confidence: 99%

“…As is well known, the role played by leukocytes in the microcirculation of subjects with chronic venous hypertension is diverse and in fact, while trapping especially concerns monocytes, activation involves granulocytes [13]. An increase in lactoferrin level has also been demonstrated during acute experimental venous hypertension in normal subjects [7] and increased plasma elastase levels have also been found in subjects with some venous diseases, although this increase was not dependent on granulocyte count [8].…”

Section: Introductionmentioning

confidence: 99%

Deep Venous Thrombosis: Leukocyte Rheology at Baseline and after in vitro Activation

LoPresti¹,

Ferrara

Canino³

et al. 2000

Pathophysiol Haemos Thromb

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We evaluated leukocyte rheology, expressed as leukocyte filtration, polymorphonuclear (PMN) membrane fluidity and cytosolic Ca²⁺ concentration in subjects with acute deep venous leg thrombosis (DVT). In 14 subjects with leg DVT we examined the leukocyte filtration [unfractionated, mononuclear cells (MN), PMNs], PMN membrane fluidity and PMN cytosolic Ca²⁺ concentration. Subsequently, we evaluated the same PMN variables after in vitro chemotactic activation with 4-phorbol-12-myristate-13-acetate. At baseline, we observed a significant difference in the filtration of unfractionated and MNs and in PMN cytosolic Ca²⁺ concentration. After PMN activation, a significant variation, greater in DVT subjects, was present in PMN filtration at 5 and 15 min. In normals, no variation was present in PMN membrane fluidity or cytosolic Ca²⁺ concentration after activation, while in subjects with DVT we found a significant variation in both PMN parameters. These results underline that there is a systemic leukocyte functional alteration in DVT.

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“…Under chronic conditions of venous pressure elevation, a number of indicators of inflammation can be detected (7,23), including endothelial adhesion molecule expression (22), release of proteolytic enzymes (26), and the presence of leukocyte migration into valve tissue and the venous wall (19,25). The trigger mechanisms that lead to development of the inflammatory reaction in venules with leukocyte and endothelial activation remain incompletely defined.…”

mentioning

confidence: 99%

Enhancement of reperfusion injury by elevation of microvascular pressures

Takase¹,

Lerond

Bergan

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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-Schö nbein. Enhancement of reperfusion injury by elevation of microvascular pressures. Am J Physiol Heart Circ Physiol 282: H1387-H1394, 2002; 10.1152/ajpheart.01003.2000.-Elevated venous pressure can be associated with severe tissue injury. Few links, however, between venous hypertension and tissue damage have been established. We examined here the effects of micropressure elevation on the outcome of venular occlusion/reperfusion in the mesenteric microvasculature of male Wistar rats. One hour of venular occlusion (diameter ϳ50 m) by micropipette occlusion followed by reperfusion were carried out with sham surgery without occlusion as control. Leukocyte rolling, adhesion, and migration, oxygen radicals detected by dichlorofluorescein (DCF), and parenchymal cell death detected by propidium iodide (PI) were recorded simultaneously in the same vessel at a location upstream of the occlusion site with elevated micropressure and at a downstream location with low micropressure. The number of rolling, adhering, and migrating leukocytes increased on the upstream side of the occlusion to a higher level than downstream of the occlusion site. During occlusion, DCF intensity on the venular endothelium was greater on the upstream side than in the downstream side, but there were no differences during reperfusion. The number of PI-positive cells adjacent to the venules increased significantly compared with controls, and it remained greater on the upstream higher-pressure side than the downstream side. Leukocyte adhesion and transvascular migration in postcapillary venules as well as parenchymal cell death could be significantly reduced by the hydroxyl radical scavenger dimethylthiourea. Microhemorrhages of blood cells into the mesentery interstitium were observed only on the upstream side of the occlusion. These results indicate that an elevation of the venular blood pressure during occlusion/ reperfusion exacerbates the inflammatory cascade and tissue injury. Venous occlusion may constitute an important mechanism for tissue injury. rat mesentery; venules; free radicals; cell death; leukocytes; endothelium; propidium iodide; 2Ј,4Ј-dichlorodihydrofluorescein; venous hypertension; microhemorrhage PRIMARY AND SECONDARY VENOUS INSUFFICIENCY is characterized by destruction of venous valves and elevation of venous pressure. Under chronic conditions of venous pressure elevation, a number of indicators of inflammation can be detected (7, 23), including endothelial adhesion molecule expression (22), release of proteolytic enzymes (26), and the presence of leukocyte migration into valve tissue and the venous wall (19,25). The trigger mechanisms that lead to development of the inflammatory reaction in venules with leukocyte and endothelial activation remain incompletely defined.There is now a large body of evidence to suggest that temporary arterial occlusion followed by reperfusion leads to an inflammatory cascade with cell activation and injury (for a recent review, see Ref. 3). Mainly, such studies have been carried out with occlusi...

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Plasma elastase in venous disease

Cited by 69 publications

References 30 publications

Neutrophil Activation and Mediators of Inflammation in Chronic Venous Insufficiency

Neutrophil Activation and Mediators of Inflammation in Chronic Venous Insufficiency

Deep Venous Thrombosis: Leukocyte Rheology at Baseline and after in vitro Activation

Enhancement of reperfusion injury by elevation of microvascular pressures

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