Article Text

  1. CTD Lee1,
  2. MS Whiteley1,2,
  3. JM Li1
  1. 1Faculty of Health and Medical Sciences, University of Surrey
  2. 2Whiteley Clinic, Guildford, UK


Endothelial dysfunction, smooth muscle cell hypertrophy and extracellular matrix disruption have been found to be involved in the pathogenesis of vein structural damage and blood stasis. However, the mechanisms which underlie these changes remain under-investigated. We hypothesised that increased reactive oxygen species (ROS) production and inflammation may play a crucial role. In this study, we examined the differences in the levels of inflammatory cell infiltration, ROS production and smooth muscle cell migration in grossly dilated, hypertrophic and normal structured vein sections obtained from the same patients. The possible enzymatic source of ROS production was also investigated.

The histopathological examination by H&E staining revealed that grossly dilated sections had much thinner walls with media dystrophy as compared to normal structured sections. Even within sections of apparently normal veins, areas of intimal thickening and inflammation were seen with smooth muscle cell migration from the media to the intima. In such areas, prominent expression of NOX2 and macrophage infiltration was seen using immunohistochemistry. Accompanied with the vessel inflammatory response, there was approximately two-fold increase in superoxide production in dilated sections as compared to normal controls (p<0.05) as detected by lucigenin (5 µM)-enhanced chemiluminescence.

In conclusion, oxidative damage may contribute to the appearance of localised dilated sections of vein which showed much thinner walls. Furthermore, intimal thickening and inflammation in grossly normal sections suggest a complex pathophysiology resulting in different abnormalities along the whole length of vein and may represent an intermediate stage in the development of abnormal, dilated varicosities.

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