INTRODUCTION:Programmed cell death plays a critical role in various physiological processes. In the present study, we investigated its possible pathogenic role in primary varicose veins. We studied histological changes in surgical specimens from thrombophlebitic saphenous veins. In thrombophlebitic saphenous, varicose, and healthy veins, we also determined the number of apoptotic cells, and investigated apoptosis in the role of the pathogenesis of varicose veins. METHODS:Forty-four specimens of thrombophlebitic saphenous veins and simple varicose veins were collected. Thirteen samples of normal great saphenous veins were also collected (control group). Apoptosis of venous walls was determined by terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) and immunofluorescence methods. The corpuscular number per high-power field was counted under light microscopy. RESULTS:A significantly higher apoptotic ratio of the intima and media were observed in control veins as compared with thrombophlebitic saphenous veins and simple varicose veins (p < 0.01). A significant difference was not observed between thrombophlebitic saphenous veins and simple varicose veins (p > 0.05). A significant difference was not seen between the intima and media of the three groups (p > 0.05). CONCLUSION:In the walls of thrombophlebitic saphenous veins and varicose veins, the apoptotic indices were clearly decreased. The results suggest that the process of programmed cell death was inhibited in walls of thrombophlebitic saphenous veins and varicose veins.

Objective Disordered programmed cell death may play a role in the development of superficial venous incompetence. We have determined the number of cells undergoing apoptosis and the alterations in the apoptotic level in the wall of different segments of the great saphenous varicose vein.Methods Twenty-one varicose great saphenous veins (VGSVs) (varicose group) and 12 normal great saphenous veins (GSVs) (control group) were collected, and the apoptosis level in the upper, middle, and lower segments were immunohistochemically stained with antibodies (anti-Bax and anti-Bcl-xl). Apoptosis was evaluated by the TUNEL assay and immunofluorescence staining. The morphology of apoptotic cells was observed with an electron microscope.Results Quantitative analysis showed that the apoptotic ratios in venous walls (intima and media) of the varicose group were significantly lower than the corresponding regions in the control group (all P<0.05). A significantly higher apoptotic rates of the venous walls was observed in control group within the upper compared with the lower segment (P<0.05). Significantly higher positive proteins expression rates of Bcl-xl/Bax were also detected in the VGSVs compared with the GSVs within the three segments, respectively (P<0.01). Electron microscopic observations confirmed that endothelial and smooth muscle cells in varicose and normal vein walls exhibited apoptotic morphologic features, such as fuzzy mitochondrial cristae, medullary changes, and margination of the nuclear chromatin.Conclusion VGSV walls were found to have a significant decrease in apoptotic rate compared with that of GSVs. The rate of apoptosis in the intima and media within the upper segment was increased more than the middle and lower segments in the GSVs. Our findings confirm that programmed cell death is down-regulated in primary varicose veins.

BACKGROUND:Following splenomegaly due to portal hypertension, pathologic characteristics include passive congestion and lymphoplasia. High venous pressure and hemodynamics can result in vascular proliferation and lymphoplasia, and promote splenic microcirculation and functional changes. The aim of this study was to determine the changes in penicillar arterioles (PAs) of red pulp in residual splenic tissue after subtotal splenectomy due to splenomegaly in cirrhotic patients to provide anatomic and physiologic evidence for reserved splenic surgery.METHODS:Thirteen patients with splenomegaly due to portal hypertension, who were treated surgically, comprised the splenomegaly group. After 8 years, we obtained another specimen by puncture biopsy from the residual spleen group. We designated patients with splenic trauma as the control group. The morphology of PAs under light microscopy was facilitated by EVG staining and immunohistochemistry for CD34. Semi-thin sections were HE-stained. The ultrastructure of PA endothelial cells was observed under electron microscopy.RESULTS:In the residual spleen group, diffuse distribution, tenuous elastic intima in the arterial wall, and continuity in PA of red pulp were seen under light microscopy. A significantly lower density and average cross-sectional area of PAs were observed in the residual spleen group compared with the splenomegaly and control groups (P < 0.01). A uniform mitochondrial matrix and a decreased number of ruptured cristae in PA endothelial cells were observed under electron microscopy. While there were some beneficial changes (splenic artery flow volume, portal venous diameter, and portal venous flow volume), the platelet and leucocyte counts were markedly increased in residual spleen.CONCLUSION:Subtotal splenectomy can eliminate the factors which precipitate splenomegaly (portal hypertension), improve the reconstruction of splenic capillaries, correct hypersplenism, and restore normal splenic function.

Background: Portal hypertension (PHT) requires invasive measures to prevent rupture and bleeding of esophagogastric varices; however, the long-term results of subtotal splenectomy plus fixation of the retrosternal omentum majus (SSFROM) have not been reported. Specifically, the advantages and disadvantages of surgery that preserves the spleen and the long-term hematologic effects have not been described.Study design: Our studies relating to SSFROM commenced in February 1999. As of April 2014 we have performed 256 subtotal splenectomies The records of 65 patients with PHT who underwent SSFROM were reviewed retrospectively.Results: Four patients died within 4 years of surgery, with a 4-year survival rate of 94 %; the 11-year survival rate was 60 %. Eleven patients (17 %) had re-bleeding from esophagogastric varices. The white blood cell and platelet counts were higher 6 and 11 years post-operatively compared with pre-operative values (P < 0.01). Portal venous diameter, portal venous flow volume, splenic artery flow volume, as well as splenic length, thickness, and average cross-sectional areas were shown to be significantly constricted or decreased (P < 0.01). The proportion of serum CD3+ T cells, CD4+ T cells, and CD8+ T cells was increased (P < 0.01), while the serum levels of macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor were significantly decreased (P < 0.01). There was no significant change in the serum levels of IgA, IgM, IgG, and Tuftsin (P > 0.05). DSA demonstrated that 15 cases formed collateral circulations between the portal vein and superior vena cava.Conclusion: SSFROM provide long-term hemostasis for esophagogastric variceal bleeding in PHT and corrected hypersplenism. SSFROM is an effective treatment for patients with PHT in whom long-term survival is expected.