Aim: Studies have shown that the incidence and development of pathological changes in the walls of the great saphenous vein and splenic vein are closely related to high venous pressure. Such changes are referred to as "vascular adaptive remodeling responses under high venous pressure". The proposition of the concept of vascular remodeling contributes to our knowledge of pathological changes in the venous wall (dilation of the venous lumen and thickening of the venous wall). In the present study, we compared the histomorphology and cytomorphology of the walls of varicose great saphenous veins (GSVs) and diseased splenic veins (SVs) to investigate the remodeling of the venous wall under high hemodynamic pressure.
Methods: We collected 34 samples of varicose great saphenous veins and diseased splenic veins. Thirty-four samples of normal great saphenous veins and splenic veins were also collected (control group). Samples were made into slices and observed under light microscopy and electron microscopy. The thickness of the tunica intima and tunica media as well as the inner diameter of the venous lumen were measured.
Results: Under light microscopy, the walls of varicose veins stained with H&E were unevenly thickened, and those of diseased splenic veins were evenly thickened; mucoid degeneration of the tunica intima of varicose veins was not obvious by Masson staining (2/20 cases). The boundary between the tunica intima and tunica media was clearly defined. Uneven hyperplasia of muscular connective tissues was observed. For the diseased splenic-vein group, mucoid degeneration of the tunica intima was obvious (8/14 cases), with an unclearly defined boundary between the tunica intima and tunica extima. Uneven hyperplasia of muscular connective tissues was also observed. Differences in the thickness and inner diameter of the tunica intima and tunica media between the great saphenous vein and the splenic vein were significantly different. Under electron microscopy, mitochondrial degeneration in endothelial cells was observed in both groups. Increased numbers of rough endoplasmic reticula in the cytoplasm of smooth muscle cells, ribosomes and mitochondria and decreased numbers of myofilaments were also observed.
Conclusion: High hemodynamics affected the remodeling of varicose great saphenous veins and diseased splenic veins. The histomorphology of visceral veins showed more significant pathological changes than that of peripheral veins. Similar cytomorphological changes were observed in both groups.