Venous stasis causes release of interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF alpha) by monocyte-macrophage

Citation
Ss. Signorelli et al., Venous stasis causes release of interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF alpha) by monocyte-macrophage, CL HEMORH M, 22(4), 2000, pp. 311-316
Citations number
26
Categorie Soggetti
Hematology,"Cardiovascular & Hematology Research
Journal title
CLINICAL HEMORHEOLOGY AND MICROCIRCULATION
ISSN journal
13860291 → ACNP
Volume
22
Issue
4
Year of publication
2000
Pages
311 - 316
Database
ISI
SICI code
1386-0291(2000)22:4<311:VSCROI>2.0.ZU;2-P
Abstract
Background: many studies have investigated between venous stasis, functions of the vascular and perivascular anastomotic structure, venous endothelium and circulating leukocytes. Setting: patients with varicose veins (n = 15) and a healthy control group (n = 15). Methods: the authors investigated so me soluble mediators of monocytes-macrophages, which induce inflammation. T hey determined interleukin 1 beta (IL-1 beta) and interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF alpha) levels at rest and after induced ve nous occlusion (using an inflated cuff to 60 mmHg for 25 minutes). Results: their results revealed elevated baseline production in the former and that induced venous occlusion further augmented the levels of all cytokines in the study series, especially in patients with varicose veins. Conclusion: T he authors believe that the study shows functional activation of monocyte-m acrophages related to venous stasis as a consequence of venous hypertension . Cell response damages the endothelial structure and may represent an impo rtant element in the pathophysiology of chronic venous insufficiency.