The Study On The Ureter Ultrastructure And Expression Of SKca In The Ureter Smooth Muscle Cell Of The Neuropathic Urinary Tract Dysfunction Rats

Objective: Neurogenic urinary tract dysfunction(neurogenic urinary tract dysfunction, NUTD) refers urination associated with nervous system damage. Improving the quality of life and the protection of upper urinary tract function is the treatment principles of urinary tract dysfunction. However, in the long-term clinical work we found that there are still patients develop with upper urinary reflux damage. Although they have treated with detrusor injection of botulinum toxin type A, anticholinergics, the clean intermittent catheterization, autologous intestinal bladder augmentation or bladder augmentation to increase bladder capacity and compliance. The change of ultrastructural, especially changes in mitochondria play an important role in the smooth muscle contraction. The small conductance calcium-activated potassium channels(small-conductance Ca2 +-activated K + channels, SKca) in the regulation of smooth muscle cell excitability the role is also critical. However the changes of NUTD ureteral smooth muscle cells ultrastructural and SKca not entirely clear. In order to comprehensive grasp on NUTD urinary tract dysfunction mechanism, we detect the expression on the rats with NUTD by the Skca of ureteral smooth muscle cells and the ultrastructural changes. We believe that the study will provide a new method for the prevention of reflux and upper urinary tract damage occurring of NUTD patients.Method: 1, Select 45 SD female rats weighing 200±20g, provided by the Experimental Animal Center of Zhengzhou University, regular feeding 20 d until rats adapt to the environment. Then randomly divided into experimental group(the NUTD group), experimental control group(the EC group), blank control group(the BC groups). Meanwhile the fine structure of ureter smooth muscle cell were objected by electron microscopy.(1)The BC group was without any operation, the video-urodynamic was used to confirmed the BC group have normal urinary function.(2) We operated the rats in NUTD group to destroyed the sacral cord by transection at the first lumbar level.The video-urodynamic test was played one week later to ensure that the NUTD group existed acontractile detrusor(ACD) and no increased bladder capacity and vesicoureteral reflux(VUR).(3) EC group: the rats of EC group was only bited the first lumbar, but not damage the spinal cord. One week later video-urodynamic was played to assessment no significant bladder and urethra dysfunction. 2, Six weeks later the model rats underwent ureter functional assessment, morphology and specimen production. 3,The technology of western blot and real-time fluorescent quantitative PCR was used to measure the expression of m RNA and protein of SKca in ureter smooth muscle cell(USMC). 4, the use of electron microscopy to observe the ultrastructure of the ureterResult: 1. Six weeks later after the operation the rat of in NUTD groups were showed no detrusor overactivity and shrinkage. 2. The urine produced by NUTD group in 30 min was(0.90 ± 0.17) ml, EC group(0.86 ± 0.18) ml, BC group(0.94 ± 0.15) ml.And three was not statistically significant difference among the groups, but NUTD group ureteral peristalsis frequency(16.23 ± 2.35) times / 5min significantly lower than EC group(21.80 ± 1.97) times / 5min and BC group(20.47 ± 2.48) times / 5min(P <0.05). in SKca2 and SKca3 m RNA expression of USMC in NUTD group relative to the BC group were up an average of 4.15 and 4.56 fold(P <0.01), protein expression was also significantly increased(P <0.01). 3. There is no obvious changes of USMC in the three groups of ureter epithelium, lamina propria and muscle morphology under light microscope, And also without congestion, edema and inflammatory cell infiltration. 4. We observed under the electron microscope that the USMC scattered arrangement in NUTD group, the mitochondrial volume increasing and edema, the number of mitochondria increased and thickening, medullary change. Some cells can also be seen extensive damage to the inner mitochondrial membrane and cristae membrane.Conclusion: 1. We induced that the rats with NUTD has primary dysfunction. 2. The increase of the SKca2, SKca3 expression in USMC of the rats with neurogenic urinary tract dysfunction may be one of the causes of ureteral motility dysfunction. 3. The ultrastructural changes of USMC may be a direct result of its primary factors dysfunction.