脊髓损伤后大鼠阴茎组织中神经型一氧化氮合成酶的变化

关键词：脊髓损伤  阴茎  神经型一氧化氮合成酶  勃起功能障碍

Keywords:spinal cord injury  penis  neuronal nitric oxide synthase  erectile dysfunction

摘要：

      目的：观察SD大鼠脊髓损伤(SCI)后阴茎组织中神经型一氧化氮合成酶（nNOS）的变化。方法： 12只雄性SD大鼠分为SCI组与对照组。采用改良的重物坠落法（Allen法）制作大鼠T9-T10脊髓节段不完全损伤模型。伤后7天行阴茎勃起功能检测和nNOS免疫组化，观察脊髓损伤后阴茎勃起潜伏期、勃起次数以及阴茎组织中nNOS神经纤维的变化。结果：SCI 组大鼠阴茎勃起潜伏期明显缩短，阴茎勃起次数明显减少（P<0.05）；对照组和SCI组大鼠阴茎中nNOS阳性神经纤维数目分别为90.42±3.66、10.13±1.78；平均光密度分别为0.18±0.01、0.11±0.01；积分光密度分别为2.37±0.08、1.08±0.13。与对照组相比较，SCI组大鼠阴茎内nNOS 阳性纤维的数量及光密度明显降低，差异具有显著性意义（P<0.05）。结论：SD大鼠脊髓损伤后阴茎内nNOS表达减弱，导致勃起功能障碍。

Abstract:

      Objective: To observe the changes of neuronal nitric oxide synthase(nNOS) in the penis of spinal cord injury(SCI) rats. Method: Twelve male SD rats were divided into SCI（T9-T10） group and control group. The incomplete SCI model was induced by using modified Allen′s method. After SCI 7d, all experimental rats were measured for the correspondent penile erections，and sacrificed for detection of nNOS-containing nerve fibers in the penis by immunohistochemistry. Result: Compared with control group， there was significant reduction of latency of erection，the numbers of erection, and nNOS-containing nerve fibers in the penis of SCI rats(P<0.05). Conclusion: The appearance of erectile dysfunction after SCI may be caused by the decrease of nNOS expression in penis.