ObjectiveTo interpret the mechanisms of vascular repair disorders in steroid-induced avascular necrosis of the femoral head (SANFH) via detection of the changes of proliferation, migration, and macrophage migration inhibitory factor (MIF)/vascular endothelial growth factor (VEGF) expressions of endothelial cells (ECs) under hypoxia/glucocorticoid. MethodsAccording to culture conditions, human umbilical vein ECs (HUVECs) at passage 3 were divided into group A (normal), group B (1.0×10-6 mol/L dexamethasone), group C (hypoxia), and group D (hypoxia+1.0×10-6 mol/L dexamethasone). The cell activity was detected by AlamarBlue; the number of viable cells was detected in live/dead cell staining; the cell morphology was observed after cytoskeleton staining; cell migration ability was compared by scratch test; and the levels of MIF and VEGF expressions were detected by ELISA. ResultsAt 24 hours after culture, the cell activity and the number of living cells in group C were significantly higher than those in the other 3 groups, showing significant difference between groups (P < 0.05), and group D had the worst cell activity and least living cells. Cytoskeleton staining showed that cells had normal morphology in groups A and B; cells had rich cytoskeleton and secretion granules in group C; cytoskeleton form disorder and nucleus pyknosis were observed in group D. Scratch test showed that the cell migration ability of group C was strongest while cell migration ability of group D was weakest. Accumulated concentration of MIF and VEGF in 4 groups significantly increased with time extending. Accumulated concentration of MIF in group C were significantly higher than that in other 3 groups at each time point (P < 0.05). Within 24 hours after intervention, stage concentration of MIF during 1-8 hours was significantly lower than that during 0-1 hour and 8-24 hours in every group (P < 0.05). Stage concentration of MIF in group C was significantly higher than other groups during 0-1 hour and 8-24 hours (P < 0.05). Within 2 hours after intervention, stage concentration of MIF in 4 groups during 0.5-1 hour was significantly higher than that during other stages (P < 0.05). Accumulated concentration of VEGF in group C was significantly higher than that in other groups at 8 and 24 hours (P < 0.05). The stage concentration of VEGF in groups C and D during 8-24 hours was significantly higher than that during 0-1 hour and 1-8 hours (P < 0.05). There was no significant difference in the stage concentration of VEGF within and among group A, B, C, and D at every stage within 2 hours after intervention (P > 0.05). ConclusionIn hypoxia environment, the proliferation and migration of ECs is enhanced, and the secretion of VEGF and MIF is increased. High concentration of dexamethasone will suppress the process above, which induces vascular repair disorders and aggravating SANFH.
Objective To summarize the clinical experience of vascular repair and reconstruction for treating superior vena cava syndrome (SVCS) caused by thoracic tumor. Methods Between October 2008 and June 2016, 26 patients with thoracic tumor and SVCS were admitted. There were 18 males and 8 females, aged from 27 to 70 years (mean, 45.9 years). Tumor was typed as B1-B3 thymoma in 13 cases, thymic carcinoma in 6 cases, large B-cell lymphoma in 3 cases, T lymphocytic lymphoma in 1 case, malignant teratoma in 1 case, right lung squamous cell carcinoma in 1 case, and carcinoid in 1 case. The tumor diameter ranged from 8 to 15 cm with an average of 10 cm. The patients had different degrees of neck, face, and upper extremity edema, jugular vein distention, and chest wall collateral venous filling. The superior vena cava pressure was 2.45-5.39 kPa. After excision of tumor and invading superior vena cava, 7 patients underwent superior vena cava reconstruction and 19 patients underwent artificial vascular replacement. Results There was no perioperative death, and the symptoms of superior vena cava obstruction were eliminated. Postoperative pulmonary infection, respiratory muscle weakness, and right chylothorax occurred in 4 cases, 1 case, and 1 case respectively. Twenty-four patients were followed up 2-92 months (mean, 37 months), and 2 patients failed to be followed up. At 1, 3, and 5 years, the survival rate was 83.3% (20/24), 41.7% (10/24), and 25% (6/24), respectively. In 6 patients with 5-year survival, there were 1 case of type B1 thymoma, 3 cases of type B3 thymoma, and 2 cases of large B-cell lymphoma. Conclusion For preoperative evaluation of SVCS caused by resectable thoracic tumors, vascular repair and recons-truction technique can be used to quickly and effectively relieve the clinical symptoms and improve the quality of life.