中文摘要：

背景随机的拍动是在改造外科的一个种最广泛地使用的皮肤拍动；然而，它的远侧的结束的部分坏死现在仍然是一个重要问题。这研究的目的是评估组织缺氧 preconditioned 骨头髓的效果间充质的在间充质的干细胞( nBMSCs )是的 rats.Methods Normoxic 骨头髓的极端长的随机的皮拍动幸存上的干细胞( HpBMSCs )移植在 normoxia (20% O2 )和在组织缺氧(1% O2 )下面的 HpBMSCs 下面有教养为在移植前的 48 个小时。三十只 Sprague-Dawley 老鼠随机与每由 10 组成被划分成控制组， nBMSCs 组和 HpBMSCs 组老鼠。极端长的随机的皮拍动在上的幸存区域老鼠背面被测量在拍动外科和房间移植以后的七天。在 vivo ， microvessel 密度和脉管的 endothelial 生长因素( VEGF )的房间幸存被组织学的检查和连接酶的 immunosorbent assay.Results 与另外的二个组相比评估，在 HpBMSCs 组的拍动幸存区域显著地更大( P 0.05 )在 HpBMSCs 组( 36.20+8.19 )的 .Microvessel 密度在 nBMSCs 组比那高( 30.01 ??湡?牧畯??猠?慷?桴?数'詼b敧漠? 敮瑵潲桰汩s

英文摘要：

Background Random flap is one kind of the most widely used skin flaps in reconstructive surgery; however, partial necrosis of its distal end remains a significant problem now. The aim of this study was to evaluate the effect of hypoxia preconditioned bone marrow mesenchymal stem cells （HpBMSCs） transplantation on ultra-long random skin flap survival in rats. Methods Normoxic bone marrow mesenchymal stem cells （nBMSCs） were cultured under normoxia （20% 02） and HpBMSCs under hypoxia （1% 02） for 48 hours before transplantation. Thirty Sprague-Dawley rats were randomly divided into control group, nBMSCs group and HpBMSCs group with each consisting of 10 rats. Survival area of ultra-long random skin flap on the dorsal of rats was measured seven days after flap surgery and cell transplantation. Cell survival in vivo, microvessel density and vascular endothelial growth factor （VEGF） were evaluated by histological examination and enzyme-linked immunosorbent assay. Results Compared with other two groups, flap survival area in HpBMSCs group was significantly larger （P 〈0.05）. Microvessel density in HpBMSCs group （36.20-.8.19） was higher than that in nBMSCs group （30.01-.5.68） and control group （17.60..4.19） （P 〈0.05）. VEGF in HpBMSCs group （（300.05-.50.41） pg/g） was higher than those in nBMSCs group （（240.55_＋33.64） pg/g） and control group （（191.65..32.58） pg/g） （P 〈0.05）. Conclusion HpBMSCs transplantation improves ultra-long random skin flap survival via promoting angiogenesis of more survival cells.