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Objective To probe the etiology and management of restenosis after artificially grafting bypass for chronic ischemia of the lower extremities. Methods In this study 52 cases suffering from postoperative restenosis and obliteration were compared with 32 cases whose artificial grafts remain patent during the same postoperative follow-up period of 3～62 months.Possible risk factors that lead to restenosis were evaluated.Resuits FIB(4.48±1.68)g/L,CRP(9.5±2.6)mg/L and LDL(4.5±1.7)mmol/L were significantly higher in the restenosis group than FIB(3.50±0.72)g/L,CRP(4.0±3.2)mg/L and LDL(2.8±0.9)mmol/L in the patent group(P＜0.01).There were no significant difference between HDL(1.02±0.32)mmol/L in the restenosis group and HDL(1.12±0.28)mmol/L in the patent group (P＞0.05).Reoperation in these 52 cases found severe intima hyperplasia and secondary thrombosis within anastomosis in 42 cases and the remaining 10 cases were found with artificial vessel primary thrombosis.After reoperation,artificial graft remain patent in 28 cases,limb amputation was performed in 10 cases,the grafted bypass were removed due to infection in 3 cases. Five patients died postoperatively.Conclusion The main reason for restenosis after artificially grafting bypass is intima hyperplasia in vascular anastomosis.Higher levels of FIB,CRP and LDL maybe the major high risk factors that lead to intima hyperplasia and artificial graft obliteration.
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Objectives:To investigate the effect and mechanism of adventitia applied slow-releasing triptolide on proliferation and apoptosis of VSMCs of the autologous vein graft. Methods:Twenty-four healthy rabbits were made external jugular vein to common carotid artery models and then were divided into 3 equal groups at random:Blank-control group received no management on adventitia of the vein graft;F-127 pluronic gel control group received local application of 0.5 ml 20% F-127 pluronic gel containing 0.1ml DMSO on adventitia;and experimental group received local application of 0.5 ml F-127 pluronic gel containing triptolide 300?g on adventitia. Vein graft samples were harvested at 2 weeks after the operation. Histomorphologic methods were used to detect the degree of intima hyperplasia of the samples. The expressions of proliferating cell nuclear antigen(PCNA) and bcl-2 of the samples were detected by immunohistochemistry. The apoptosis of vascular smooth muscle cells(VSMC) was detected by TUNEL. Results:Two weeks after vein grafting, compared with blank-control group and F-127 control group,intima hyperplasia was markedly inhibited by applying triptolide 300?g on adventitia(P
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Objective To observe the effects of co-transfection of proto-oncogene c-myc antisense oligodeoxynucleotides(c-myc-AODN) and tissue-type plasminogen activator(tPA) gene on intimal hyperplasia of auto-transplantion artery in rabbit. Methods The left and right external iliac artery(length 1.0 cm) of rabbits were cross transplanted. The artery grafts and sutures were respectively soaked in Lipofection, c-myc-AODN, pBudCE4.1/tPA, c-myc-AODN and pBudCE4.1/tPA solution for 15 minutes. Each group were divided into five subgroups(n=5, in each subgroup) according to the sacrifice times(3, 7, 14, 28 and 56 d after operation). Specimens were harvested for pathology, chromogenic substrate test, 3H-TdR incorporation test and immunochemisty coloration study. Result The intimal area, stenosis ratio, 3H-TdR incorporation, PCNA positive cell in c-myc-AODN adding tPA co-transfection group were significantly lower than that of control group(P0.01), and that were lower than c-myc-AODN transfection group and tPA gene transfection group(P0.05). Conclusion Vascular local co-transfection of tPA gene and c-myc-AODN effectively inhibits the proliferation of vascular smooth muscle cell(VSMC) and hyperplasia of intima of the transplanted artery.
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Objective To investigate the inhibitory effect of appling slow-releasing triptolide on adventitia on the intima hyperplasia of autologous vein graft.Methods In 24 male New Zealand rabbits, external jugular vein to common carotid artery models were established, and then were divided into 3 equal groups at random: blank-control group, receiving no management on adventitia of the vein graft; F-127 control group, receiving local application of 0.5 mL of 20 % F-127 on adventitia of the vein graft; experiment group, receiving local application of 0.5 mL of 20 % F-127 containing triptolide 300?g. Vein graft specimens were harvested at 2 weeks after the operation. Histomorphologic methods were used to detect the degree of intima hyperplasia of the specimens. The expression of bcl-2 and Fas of the specimens was detected by immunohistochemistry. The apoptosis vascular smooth muscle cells (VSMC) were detected by TUNEL.Results Two weeks after vein grafting, compared to blank-control group and F-127 control group, intima hyperplasia of experiment group [intima thickness (29.9?7.6)?m, I/M 0.56?0.08] was markedly inhibited (P
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Objective To study the effet of ET-1 and ECE on endothelial proliferation of autografted vein.Methods An animal model of the autogenous vein graft was established in 80 Wistar rats.The expression of ECE and EF-1 gene was determined by RT-PCR and immunohistological method to test the mRNA and protein expresion level respectively.Results PCNA positive smooth muscle cells appeared 6 hours after transplantation,increased with time,and reached a peak at 1 to 2 weeks.After 2 weeks,PCNA positive SMC in the tunica media began to decline and recovered to the 6 hour level at 8 weeks after the operation.mRNA of ECE increased with the time after the operation,reached a peak after 1-2 weeks,declined afterwards,and became stable at around 8 weeks.Expression change of ET1 was similar to the change of ECE,reached the peak after 1-2 weeks and was stable after 8 weeks(r=0.975).Conclusions The time and pattern of change of the pathologic process of intimal hyperplasia are in agreement with the expression of ET-1 and ECE,and suggests that ECE is involved in the process of intimal hyperplasia of vein graft.
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AIM To establish a model of vascular intima hyperplasia for study the restenosis after angioplasty. METHODS Carotid artery of rat was exposed under general anesthesia. Two pieces of steel slides(13 mm?5 mm?1 mm) were set on and under the carotid artery separately. Then the slides were squeezed by two surgical forceps paralleling to the artery for 25 min. Histomorphological study was performed at the second hour or on the fourteenth day after operation. RESULTS At the second hour after operation, the loss of endothelial integrity and platelet deposition were seen under the scanning electromicroscopy. Under the light microscopy, there were infiltration of inflammatory cells in vessel wall andthrombus formation in the vessel cavity. At the fourteenth day after operation, PCNA positive cells in vessel wall of squeezed artery were significantly higher, the ratios of intima, medium and intima areas of squeezed artery were significantly increased and the ratio of cavity area of squeezed artery was significantly decreased compared with those of uninjured artery.The vascular intima hyperplasia and PCNA positive cells in squeezed arterial wall were inhibited by oral administration of heparinoid and aspirin. CONCLUSION With squeezing carotid artery in rats the vascular intima hyperplasia as restenosis after angioplasty was established.