Optimal timing of operation for repairing atonic bladder after medullary cone injury: an experimental study in rats.
OBJECTIVE
To determine optimal timing of operation for repairing atonic bladder after medullary cone injury in rats.


METHODS
I n all, 56 adult female Sprague-Dawley rats were equally randomized into seven groups: normal control group, and 4w, 6w, 8w, 10w, 12w and 16w groups after medullary cone injury, assigned as groups A-G. The model was established by sharp transaction of spinal cord at the level of L(4/5) vertebral body. Bladder weight, cross-sectional area and ultrastructure of the detrusor muscle and its neuromuscular junction (NMJ), fibrotic change, and alpha-smooth muscle antibody (alpha-SMA) expression in the detrusor muscle were examined individually.


RESULTS
Bladder weight in groups E-G was significantly increased than that in group A (P<0.05). And cross-sectional area of detrusor muscle fiber in groups E-G was significantly smaller than that in group A (P<0.05). Transmission electronic microscopy showed that the number of synaptic vesicles, mitochondria and other organelles in NMJ decreased markedly in group E. In groups F and G, NMJ further degenerated with synaptic vesicles and organelles decreased or even disappeared. Masson's stain showed that the proportion of connective tissue in the detrusor muscle of groups E-G was significantly different from that of group A (P<0.05). alpha-SMA expression in the detrusor muscle decreased with the lapse of time.


CONCLUSIONS
The 10th week after rat medullary cone injury can be regarded as the time node when the detrusor muscle and NMJ undergo changes, and therefore surgical nerve repair should be performed before this.
Department of Orthopedics, Changzheng Hospital, Second Military Medical University, Shanghai, PR China.
X-Y
XY
Zheng
C-L
CL
Hou
A-M
AM
Chen
J-F
JF
Li
Z
Z
Xu
J-H
JH
Wang
D000199:Actins / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D046529:Microscopy, Electron, Transmission / Q000379:methods; D018485:Muscle Fibers, Skeletal / Q000473:pathology / Q000648:ultrastructure; D018482:Muscle, Skeletal / Q000473:pathology / Q000648:ultrastructure; D009468:Neuromuscular Diseases / Q000209:etiology / Q000473:pathology; D009469:Neuromuscular Junction / Q000473:pathology / Q000648:ultrastructure; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000150:complications*; D013997:Time Factors; D001745:Urinary Bladder Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*
D000199:Actins; C498862:Acta2 protein, rat