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目的超长随意皮瓣局部应用VEGF,探讨外源性VEGF对超长皮瓣成活与氧自由基的相关性。方法实验于2004年11月—2005年11月在华北煤炭医学院中心实验室完成。采用SD大鼠背部3cm×10cm单蒂缺血皮瓣模型,皮下局部注射血管内皮细胞生长因子后第十二、二十四小时检测皮瓣组织的MDA和SOD含量,通过计算机图像分析技术对皮瓣成活率进行测定、微血管密度的测定、组织学检查等手段来观察内皮细胞生长因子对缺血皮瓣成活的影响并探讨其机制。结果局部应用血管内皮细胞生长因子后,第二十四小时生理盐水组MDA含量中1/3段为(5.42±1.35)nmol/mgprot,内皮细胞生长因子组中1/3段为(2.79±0.22)nmol/mgprot;SOD活力测定在生理盐水组中1/3段为(58.27±12.81)U/mgprot、远1/3段为(109.71±40.13)U/mgprot,内皮细胞生长因子组中1/3段为(116.61±19.83)U/mgprot、远1/3段为(177.07±3.41)U/mgprot;表明内皮细胞生长因子能提高SOD活力,增强对自由基MDA的清除。组织学检查发现内皮细胞生长因子能促进皮瓣组织毛细血管增生。生理盐水组微血管密度中1/3段为(25.57±0.88)个/cm2、远1/3段为(25.2±0.40)个/cm2,内皮细胞生长因子组中1/3段为(31.76±0.77)个/cm2、远1/3段为(37.26±2.97)个/cm2;说明了内皮细胞生长因子能增加中远段皮瓣组织的微血管数量。结论内皮细胞生长因子能促进缺血皮瓣成活,其机制可能与内皮细胞生长因子直接促进毛细血管新生、提高SOD表达增加对氧自由基MDA的清除间接促血管新生相关。
OBJECTIVE: To investigate the relationship between the application of exogenous VEGF and the survival of extra long flap with oxygen free radicals. Methods The experiment was performed at the Central Laboratory of North China Coal Medical College from November 2004 to November 2005. The SD rat model of 3cm × 10cm monotonous flap was used to detect the contents of MDA and SOD in the skin flap on the 12th and 24th hour after subcutaneous injection of vascular endothelial growth factor. The skin of the skin was analyzed by computer image analysis Flap survival rate determination, determination of microvessel density, histological examination and other means to observe the effect of endothelial cell growth factor on the survival of ischemic flaps and to explore its mechanism. Results After application of VEGF, the content of MDA in the 24th hour of physiological saline group was (5.42 ± 1.35) nmol / mgprot and that of the endothelial cell growth factor group was (2.79 ± 0.22) ) nmol / mgprot. The activity of SOD in the normal saline group was (58.27 ± 12.81) U / mgprot and that in the far 1/3 of the group was (109.71 ± 40.13) U / mgprot. In the endothelial cell growth factor group, (116.61 ± 19.83) U / mgprot in the third stage and (177.07 ± 3.41) U / mgprot in the far 1/3 zone, indicating that endothelial cell growth factor can increase the activity of SOD and enhance the clearance of free radical MDA. Histological examination found endothelial cell growth factor can promote capillary tissue hyperplasia. In the saline group, the microvessel density was (25.57 ± 0.88) / cm 2 in the microvessel density and (25.2 ± 0.40) cm 2 in the distal 1/3 and 31.76 ± 0.77 in the endothelial cell growth factor group ) Cells / cm2, and far 1/3 of the cells were (37.26 ± 2.97) cells / cm2. It showed that endothelial cell growth factor could increase the number of capillaries in the mid-distal flap. CONCLUSION: Endothelial cell growth factor (VEGF) can promote the survival of ischemic flap. The mechanism may be related to the direct promotion of angiogenesis by endothelial cell growth factor and the increase of SOD expression, which may be related to the indirect angiogenesis of MDA scavenging.