title: Progressive vascular damage may lead to bladder underactivity in rats.
abstract: OBJECTIVE
  We assessed whether progressive vascular damage causes bladder underactivity in rats.
  
  
  METHODS
  Adult male Sprague Dawley® rats were divided into 4 groups. Controls received a regular diet and tap water. The L-NAME group received a 2% cholesterol diet and L-NAME (3 mg/ml) dissolved in drinking water. The arterial injury group underwent balloon endothelial injury of the common iliac arteries and received a 2% cholesterol diet and tap water after injury. The arterial injury/L-NAME group also received L-NAME dissolved in drinking water. At 8 weeks urodynamics were performed, bladder tissue was harvested for pharmacological studies, and the iliac arteries and bladders were histologically examined.
  
  
  RESULTS
  Iliac arteries from the injury and injury/L-NAME groups showed neointimal formation and luminal occlusion but arteries from the L-NAME group did not. In the L-NAME and injury groups bladder capacity and voided volume were less than in controls. Conversely, in the injury/L-NAME group these cystometric parameters were significantly greater than in the other groups. Post-void residual volume in the injury/L-NAME group tended to increase compared with the other groups. Contractile responses of bladder strips to various stimuli in the L-NAME, injury and injury/L-NAME groups were significantly less than in controls and the lowest in the injury/L-NAME group. The injury and injury/L-NAME groups showed a significantly increased percent of collagen compared to controls.
  
  
  CONCLUSIONS
  Pelvic arterial occlusive disease plus vascular endothelial dysfunction may cause progressive vascular damage resulting in bladder dysfunction that develops from bladder hyperactivity to bladder underactivity.
authors.affiliation: Department of Urology, Fukushima Medical University of School of Medicine, Fukushima City, Japan. Electronic address: mnomiya44@gmail.com.
authors.forename: Masanori
authors.initials: M
authors.lastname: Nomiya
authors.affiliation: Division of Bioengineering and Lower Urinary Tract Dysfunction Research, Nihon University School of Engineering, Koriyama City, Japan.
authors.forename: Osamu
authors.initials: O
authors.lastname: Yamaguchi
authors.affiliation: Department of Urology, Fukushima Medical University of School of Medicine, Fukushima City, Japan.
authors.forename: Hidenori
authors.initials: H
authors.lastname: Akaihata
authors.affiliation: Department of Urology, Fukushima Medical University of School of Medicine, Fukushima City, Japan.
authors.forename: Junya
authors.initials: J
authors.lastname: Hata
authors.affiliation: Wake Forest Institute for Regenerative Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina.
authors.forename: Norifumi
authors.initials: N
authors.lastname: Sawada
authors.affiliation: Department of Urology, Fukushima Medical University of School of Medicine, Fukushima City, Japan.
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Kojima
authors.affiliation: Wake Forest Institute for Regenerative Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina.
authors.forename: Karl-Erik
authors.initials: KE
authors.lastname: Andersson
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications; D018450:Disease Progression; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D001745:Urinary Bladder Diseases / Q000209:etiology*; D014652:Vascular Diseases / Q000150:complications*
keywords: arterial occlusive diseases; ischemia; lower urinary tract symptoms; pelvis; urinary bladder