上海交通大学学报（医学版）

›› 2012, Vol. 32 ›› Issue (4): 379-.doi: 10.3969/j.issn.1674-8115.2012.04.001

• 专题报道（排尿功能障碍及盆底重建） • 上一篇    下一篇

一氧化氮合成酶神经化学重塑在脊髓损伤大鼠下尿路功能障碍中的机制及应用

张 帆, 廖利民   

  1. 首都医科大学康复医学院 |北京博爱医院泌尿外科, 北京 100068
  • 出版日期:2012-04-28 发布日期:2012-04-27
  • 通讯作者: 廖利民, 电子信箱: lmliao@263.net。
  • 作者简介:张 帆(1983—), 男, 主治医师, 博士生；电子信箱: zhangfan0207@126.com。
  • 基金资助:

    科技部“十一五”科技计划资助项目（2008BAI50B06）

Mechanism and application of nitric oxide synthase neurochemical plasticity in lower urinary tract dysfunction of rats with spinal cord injury

ZHANG Fan, LIAO Li-min   

  1. Department of Urology, China Rehabilitation Research Center, College of Rehabilitation, Capital Medical University, Beijing 100086, China
  • Online:2012-04-28 Published:2012-04-27
  • Supported by:

    Foundation of the Ministry of Science and Technology of China, 2008BAI50B06

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摘要：

目的 观察完全性脊髓损伤（SCI）大鼠下尿路传入神经一氧化氮合成酶（NOS）的表达及鞘内注射NOS抑制剂对SCI大鼠膀胱测压参数的影响。方法 ①选取SD大鼠24只，随机分为正常对照A组、SCI 1周组、SCI 4周组和SCI 8周组（n=6），SCI 1周组、SCI 4周组和SCI 8周组大鼠横断胸10脊髓节段建立完全性SCI模型，免疫组织化学法检测各组大鼠L6~S1脊髓节段神经型NOS（nNOS）和诱导型NOS（iNOS）的表达。②另选取SD大鼠16只，随机分为正常对照B组（n=9）和损伤组（n=7），损伤组大鼠横断胸10脊髓节段建立完全性SCI模型4周后，两组大鼠分别鞘内注射0.1 mL生理盐水、1 μmol nNOS抑制剂和1 μmol iNOS抑制剂，观察给药前后两组大鼠膀胱测压参数的变化。结果 ①SCI 1周组和SCI 4周组大鼠脊髓后角nNOS阳性表达细胞数[(5.5±2.7)/视野和（10.3±7.9）/视野]显著大于正常对照A组[(2.0±1.5)/视野]（P<0.05），SCI 8周组大鼠脊髓前角nNOS阳性表达细胞数[(6.7±1.5)/视野]显著大于正常对照A组[(4.3±1.5)/视野]（P<0.05）。②损伤组大鼠鞘内注射nNOS抑制剂后最大膀胱测压容积[（1.58±0.94）mL]显著大于给药前[(1.06±0.70) mL]（P<0.05）。结论 脊髓水平一氧化氮可能不参与正常排尿反射过程，一氧化氮相关的神经化学递质的可塑性改变与SCI后自主排尿反射的触发有关，鞘内注射药物调节脊髓水平神经化学递质的表达为SCI后下尿路功能障碍的治疗提供了新思路。

关键词: 一氧化氮合成酶, 神经化学重塑, 脊髓损伤, 膀胱测压

Abstract:

Objective To investigate the expression of nitric oxide synthase (NOS) in afferent nerve of lower urinary tract and the effect of intrathecal injection of NOS inhibitors on cystometry parameters in rats with complete spinal cord injury (SCI). Methods ①Twenty-four SD rats were randomly divided into normal control group A, SCI 1 week group, SCI 4 weeks group and SCI 8 weeks group, with 6 rats in each group, and complete SCI model was established in SCI 1 week group, SCI 4 weeks group and SCI 8 weeks group by T10 spinal segment resection. The expression of neuronal NOS (nNOS) and inducible NOS (iNOS) in L6 to S1 spinal segment in each group of rats was detected by immunohistochemistry. ②Another 16 SD rats were randomly divided into normal control group B (n=9) and injury group (n=7), and complete SCI model was established in injury group by T10 spinal segment resection. Four weeks after model establishment, intrathecal injections of 0.1 mL normal saline, 1 μmol nNOS inhibitor and 1 μmol iNOS inhibitor were performed in two groups, and the cystometry parameters were measured in two groups before and after treatment. Results ①The numbers of cells with positive expression of nNOS in spinal dorsal horn in SCI 1 week group and SCI 4 weeks group [(5.5±2.7)/visual field and (10.3±7.9)/visual field] were significantly larger than that in normal control group A [(2.0±1.5)/visual field] (P<0.05), and the number of cells with positive expression of nNOS in spinal ventral horn in SCI 8 weeks group [(6.7±1.5)/visual field] was significantly larger than that in normal control group A [(4.3±1.5)/visual field] (P<0.05). ②The maximum bladder capacity after intrathecal injection of nNOS inhibitor was significantly larger than that before treatment in injury group [（1.58±0.94）mL vs (1.06±0.70) mL](P<0.05). Conclusion Nitric oxide in spinal level may not participate in normal micturition reflex. Nitric oxide-related neurochemical changes in lumbosacral neurons participate in the emergence of spinal micturition reflex following SCI. The manipulation of nitric oxide production may help to treat lower urinary tract dysfunction after SCI.

Key words: nitric oxide synthase, neurochemical plasticity, spinal cord injury, cystometry