机构地区:[1]上海长征医院骨科,上海200003
出 处:《上海医学》2015年第4期319-322,I0003,共5页Shanghai Medical Journal
基 金:国家自然科学基金资助项目(10JC1418300)
摘 要:目的建立脊髓圆锥损伤大鼠模型,探讨失去低级中枢神经支配后膀胱组织结构和增殖活性的改变,为经神经途径膀胱功能重建提供实验依据。方法将25只Sprague-Dawley大鼠分入实验组(20只)和对照组(5只)。实验组大鼠破坏脊髓圆锥,分别于术后1、4周和3个月处死,每次4只;对照组大鼠行假手术,于术后1周处死。处死的大鼠膀胱取材,行大体形态学观察、湿重测量、H-E和苦味酸-酸性品红(VG)染色,以及增殖细胞核抗原(PCNA)免疫组织化学检测。结果脊髓圆锥损伤动物模型构建成功。实验组术后1周时的膀胱湿重与对照组的差异无统计学意义(P>0.05),术后4周时显著大于对照组(P<0.05),术后3个月时显著大于对照组和同组术后1、4周时(P值均<0.05)。实验组大鼠术后1周时可见膀胱黏膜坏死脱落,膀胱壁充血水肿,呈急性炎性反应表现;术后4周时可见结石形成,膀胱壁充血水肿,炎性细胞浸润,逼尿肌和胶原纤维增生,呈慢性炎性反应表现;术后3个月时,膀胱进一步肥厚呈巨大囊袋状,逼尿肌萎缩,纤维增生,呈现萎缩表现。实验组术后1、4周的PCNA阳性率均显著高于对照组(P值均<0.05),且术后4周显著高于术后1周(P<0.05);实验组术后3个月的PCNA阳性率与对照组差异无统计学意义(P>0.05)。结论失去中枢神经支配后,膀胱发生炎性反应、坏死、增生等一系列病理性变化,最终因组织结构严重破坏而发生萎缩。防止膀胱组织结构发生不可逆性破坏,最大限度地保护和挽救膀胱功能是膀胱功能重建的关键环节。Objective To establish animal models of conus medullaris injury in rats, and to explore the changes of tissue structure and proliferation of rat bladders after losing lower central innervations so as to provide experimental evidence for bladder function reconstruction by repairing nerve pathway. Methods Twenty-five Sprague- Dawley rats were randomly divided into experimental group (n = 20) and control group (n = 5). The conus rnedullaris of rats in experimental group were damaged, and the rats in control group received sham operation. The rats in experimental group were sacrificed at different time points after surgery ( 1 week, 4 weeks, and 3 months), and the rats in control group were sacrificed at 1 week after surgery. Bladder specimens were harvested to perform morphological observation, wet weight measurement, H-E and Van Gieson (VG) staining, and immunohistochemical detection of proliferating cell nuclear antigen (PCNA). Results The animal model with conus medullaris injury was successfully constructed. There was no significant difference in wet weight of bladder between groups one week after surgery ( P〉0. 05). Bladder wet weight of experimental group was significantly greater than that of control group 4 weeks after surgery (P〈0.05). Three months after surgery, bladder wet weight of experimental group was significantly increased as compared with those at 1 and 4 weeks after surgery and that of control group at 3 months postoperatively (all P〈0.05). One week after medullary cone injury, bladder specimens showed an acute inflammatory reaction performance: mucosa necrosis, and wall hyperemia and edema. Four weeks after injury, bladder specimens showed a chronic inflammatory performance: hyperemia and edema of bladder wail, infiltrated inflammatory cells, hyperplasia of the detrusor muscle and collagen fiber, and bladder stones formation. Three months after injury, bladder specimens showed an atrophy performance: the detrusor muscle atrophy and fiber hyperplasia; me
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