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

• Monographic report (Urinary dysfunction and pelvic reconstruction) • Previous Articles     Next Articles

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

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