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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Online ISSN 1827-1839
Chu H. 1, Yan F. 2, Zhao J. 1, Xu Y. 1, Wang T. 3, Li K. 1, Tang J. 1, Guo W. 2
1 Center of General Surgery, The 89th Hospital of People’s Liberation Army, Weifang, China;
2 Department of Pathology, Weifang Medical University, Weifang, China;
3 Department of Pathology, The 89th Hospital of People’s Liberation Army, Weifang, China
Aim: The purpose of this study was to investigate the proliferation of vasa vasorum (VV) in the walls of thrombophlebitic saphenous vein (TSV), and to evaluate the influence of high venous pressure and lack of oxygen on the VV.
Methods: The specimens of the great saphenous vein were collected: 11 primary varicose vein (PVV), 11 TSV and, as a control, eight normal great saphenous vein. Masson staining and immunohistochemistry for CD34 were used to observe the status of VV, and the number of VV were counted under light microscopy.
Results: VV of the thrombophlebitic saphenous vein group (TSVG) were clustered together in adventitia, increased linearly in media, and scattered appearance in intima, were increased partially in intima of thrombus rupturing. In TSVG, the number of VV observed in adventitia, media and intima was 16.738±7.685, 4.845±2.537, 2.448±3.030, respectively. In the primary varicose vein group (PVVG), the corresponding values were 14.280±4.440, 2.965±1.125, 0.500±0.548. And the number was 8.911±2.629, 0.150±0.424, 0±0 in the control group (CG). Significantly higher numbers of VV were observed in the TSVG as compared to the PVVG or CG (P<0.05). No significant difference was observed between intima and media (P>0.05).
Conclusion: Thrombi in varicose veins can induce proliferation of VV, which may be involved in high venous pressure and hypoxia.