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本项研究采用大耳白兔为实验动物，采用外骨膜广泛剥离、部分肌肉切除的桡骨骨折的动物模型，采用自身对照法，分成对照组、实验组。对照组不包括软组织损伤及骨膜广泛剥离的骨折模型。利用组织学、电镜及血管灌注等方法对骨折愈合微循环变化进行了观察。并将软组织损伤对骨折愈合过程中的微循环及超微结构的变化进行了分析。术后１～８周随机分批处死动物，标本观察。实验结果显示：１．１至４周毛细血管代偿性扩张较对照组差，新生毛细血管管腔狭窄、闭塞。５周后骨折处微循环开始接近正常。２．骨皮质外侧四分之一的骨细胞变性坏死比较明显。３．形成骨痂的成骨细胞活性明显降低、胶原合成不良、骨折愈合相对迟缓。此项研究显示软组织损伤及骨外膜剥离与骨折愈合过程中的微循环改变具有直接关系。软组织损伤及骨外膜剥离可加重骨折断端的缺血，导致骨折愈合过程相对迟缓。
In this study, large white rabbits as experimental animals, the use of the external periosteum widely stripped, partial muscle resection of the radial fracture of the animal model, using self-control method, divided into control group, experimental group. The control group did not include fracture models of soft tissue injury and extensive dissection of the periosteum. The changes of fracture healing microcirculation were observed by histology, electron microscopy and blood vessel perfusion. The changes of microcirculation and ultrastructure during fracture healing were analyzed with soft tissue injury. After 1 to 8 weeks, animals were sacrificed in batches and the specimens were observed. Experimental results show: 1.1 to 4 weeks capillary compensatory expansion worse than the control group, nascent capillaries stenosis, occlusion. After 5 weeks, the microcirculation of the fracture began to approach normal. 2. One-fourth of the cortical bone degeneration and necrosis more obvious. 3. The formation of callus osteoblasts significantly reduced activity, poor synthesis of collagen, fracture healing is relatively slow. This study shows that soft tissue injury and remodeling of the adventitia are directly related to changes in microcirculation during fracture healing. Soft tissue injury and periosteal dissection can increase the fracture of the fracture at the end of the fracture, leading to relatively slow fracture healing process.