Endothelial activation and response in patients with hand arm vibration syndrome

Citation
G. Kennedy et al., Endothelial activation and response in patients with hand arm vibration syndrome, EUR J CL IN, 29(7), 1999, pp. 577-581
Citations number
29
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
ISSN journal
00142972 → ACNP
Volume
29
Issue
7
Year of publication
1999
Pages
577 - 581
Database
ISI
SICI code
0014-2972(199907)29:7<577:EAARIP>2.0.ZU;2-G
Abstract
Background Hand-arm vibration syndrome (HAVS) is a form of secondary Raynau d's phenomenon (RP) of occupational origin. In other farms of RP, blood and blood vessel wall interaction is one factor in the pathophysiology. Cytoki nes and cell adhesion molecules both play an important role in this interac tion, and basal vascular tone and vasodilatation are regulated by nitric ox ide. Methods Blood flow responses to acetylcholine (ACh) and sodium nitroprussid e (SNP) and levels of soluble intercellular adhesion molecule-1 (sICAM-1) a nd the inflammatory cytokine interleukin 8 (IL-8) were measured in eight ma le patients with vibration white finger disease, which is part of HAVS, and in eight healthy matched male control subjects. Results sICAM-1 levels were statistically higher (P = 0.02, Mann-Whitney U- test) and IL-8 levels (P < 0.01, Mann-Whitney) were significantly lower in the patient group. The patients with HAVS had significantly reduced vascula r responses to SNP (P < 0.05, ANOVA). Conclusions In this study, we reveal differences in vascular responses to S NP that suggest there may be an impairment of the smooth muscle response to nitric oxide in patients with HAVS. The increase in sICAM-1 that occurs in patients with HAVS suggests that leucocyte adhesion is increased and that adherent neutrophils may contribute to the microvascular damage seen in thi s disease. The impeded flow of blood cells through the microcirculation may result in the low levels of circulating IL8 due to the cytokine binding to erythrocytes. The possible role of NO activity in HAVS warrants further in vestigation.