中文摘要：

目的观察咯利普兰（rolipram）对脊髓挫伤大鼠神经功能的影响，并从组织学层面探讨咯利普兰的神经保护作用。方法共选取雌性SD大鼠30只，采用随机数字表法将其分为实验组及对照组。利用脊髓打击器将上述大鼠制成T10脊髓挫伤模型，实验组于伤后1h内接受为期2周的咯利普兰皮下注射（每天注射2次，每次注射剂量按照每千克体重0．25mg标准），对照组则于相同时间点注射等量生理盐水。术后每周采用BBB评分评定2组大鼠后肢运动功能情况；术后第2、4、8周时每组各随机取4只大鼠进行脊髓透射电镜观察；术后第8周时每组各取3只大鼠行脊髓HE染色并置于光镜下观察。结果实验组大鼠在术后第2、3周时后肢BBB评分分别为（8．5±3．6）分和（10．7±2．6）分，明显高于对照组（4．1±3．2）分和（7．3±3．9）分；术后第8周时实验组、对照组BBB评分分别为（11．3±1．7）分、（10．1±1．8）分，组间差异无统计学意义（P〉0．05）。通过光镜观察发现2组大鼠脊髓后索处均有囊腔形成，对照组囊腔壁内可见大量胶质细胞聚集，形成致密瘢痕组织；实验组也可见胶质细胞散在分布，但其密度显著低于对照组，未见致密瘢痕组织。通过电镜观察发现，对照组脊髓受损部位在伤后2周时即出现轴膜下水肿、髓鞘板层松散、溃变、轴索空化、髓鞘增厚、轴索消失、神经细胞变性、血管周围水肿等多种改变；伤后第4、8周时则出现较多变性轴索以及吞噬了退变髓鞘的吞噬细胞和少突胶质细胞。实验组各时间点也出现类似改变，但程度相对轻微，其主要改变包括髓鞘松散、增厚或退变、轴索变性、血管增生以及少数轴索空化等。结论早期应用咯利普兰能加速脊髓损伤大鼠运动功能恢复，减轻受损髓鞘溃变、轴索空化等轴突毁损性病变和后期轴突变性，并可抑制

英文摘要：

Objective To investigate the effects of rolipram on neurofunction and the uhrastructure of the spinal cord in rats with spinal cord contusion. Methods Thirty adult, female Sprague-Dawley （SD） rats received spinal cord contusion at the T10 level. They were then randomized into an experimental group and a control group immediately after the operation. Rats in the experimental group received subcutaneous injections of 0.25 mg/kg of rolipram twice daily for two weeks. Control rats received the same dosage of 0.9% sodium chloride solution on the same schedule. The rats＇ functional recovery was evaluated using the open-field locomotion rating scale of Basso, Beattie and Bresnahan （ BBB score） , once a week within the 1st month after spinal cord injury （SCI） , and once every two weeks subsequently. The morphology of the spinal cord tissue around the lesion site was observed under the light microscope with HE staining at the 8th week postoperation, and the uhrastructure of the spinal cord was observed under the transmission electron microscope at the 2nd, 4th and 8th week postoperation. Results At the 2nd and 3rd week after SCI the experimental group exhibited significantly greater improvement in average BBB scores than the control group. However, the average BBB scores in the experimental and control groups were not significantly different at 8 weeks after SCI. Under the light microscope, cavities were observed in the posterior dorsal column near the SCI in both the experimental and control groups. However thick, condensed glial scars in the injured area were observed only in the control group. The density of glial cells decreased more in the experimental group than in the control group. Transmission electron microscopy revealed that, compared with the control group, inflammatory edema was attenuated and fewer axons were damaged at the 2nd week postoperation in the experimental group. That group also showed less axon degeneration as well as more angiogenesis at the 4th and S th week. Conclusion Rolipram ca