title: Impaired detrusor contractility in a rat model of chronic bladder ischemia.
abstract: OBJECTIVE
  To examine the effect of chronic ischemia associated with vascular disorders on bladder function, we investigated bladder contractility and changes in morphology and nerve distribution in a rat model of chronic bladder ischemia.
  
  
  METHODS
  Adult male Sprague-Dawley rats were divided into arterial endothelial injury, sham, and control groups. The injury group underwent balloon endothelial injury of the iliac arteries and received a 2% cholesterol diet. The sham group was only incised bilaterally in the inguinal region and received the 2% cholesterol diet. The control group did not undergo any procedure and received a regular diet (0.09% cholesterol). All animals were euthanized after 8 weeks. Bladders were removed and weighed, and sections were used for muscle strip contraction and histologic analyses. Cross-sections of dissected common iliac arteries were examined histologically.
  
  
  RESULTS
  Bladder contractile response and tension were significantly decreased in the injury group compared with the sham and control groups. Tissue from the injury group exhibited marked arterial occlusion with wall thickening. In the injury group, the collagen and muscle ratio (0.80 ± 0.12) was significantly greater than in the control (P = .01) and sham (P = .04) groups. Significantly fewer protein gene product 9.5 (PGP9.5)-positive nerve fibers were found in the injury group (513 ± 53) than in the control (P = .01) and sham (P = .03) groups.
  
  
  CONCLUSIONS
  Vascular occlusive disorders cause fibrosis and reduce the number of nerves innervating the bladder, which leads to decreased bladder contractility in a rat model of chronic bladder ischemia.
authors.affiliation: Department of Urology, Fukushima Medical University School of Medicine, Hikarigaoka, Fukushima 960-1295, Japan. sgwkj@fmu.ac.jp
authors.forename: Koji
authors.initials: K
authors.lastname: Sagawa
authors.forename: Ken
authors.initials: K
authors.lastname: Aikawa
authors.forename: Masanori
authors.initials: M
authors.lastname: Nomiya
authors.forename: Soichiro
authors.initials: S
authors.lastname: Ogawa
authors.forename: Hidenori
authors.initials: H
authors.lastname: Akaihata
authors.forename: Norio
authors.initials: N
authors.lastname: Takahashi
authors.forename: Osamu
authors.initials: O
authors.lastname: Yamaguchi
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Kojima
mesh_terms: D000818:Animals; D002908:Chronic Disease; D003094:Collagen; D004195:Disease Models, Animal; D005355:Fibrosis; D007083:Iliac Artery / Q000293:injuries / Q000473:pathology*; D007511:Ischemia / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000473:pathology / Q000503:physiopathology*; D009412:Nerve Fibers / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D043222:Ubiquitin Thiolesterase / Q000378:metabolism; D001743:Urinary Bladder / Q000098:blood supply* / Q000294:innervation / Q000473:pathology / Q000503:physiopathology*
chemical_list: D003094:Collagen; C489034:UCHL1 protein, rat; D043222:Ubiquitin Thiolesterase