title: Increased bladder activity is associated with elevated oxidative stress markers and proinflammatory cytokines in a rat model of atherosclerosis-induced chronic bladder ischemia.
abstract: OBJECTIVE
  To further characterize, in a rat model, the effects of atherosclerosis-induced chronic bladder ischemia on bladder function and associated changes in oxidative stress markers and proinflammatory cytokines.
  
  
  METHODS
  Adult Sprague-Dawley male rats were divided into three groups (arterial endothelial injury: AI, sham, naïve). The AI group (n = 14) underwent endothelial injury of the iliac arteries and received a 2% cholesterol diet. The sham group (n = 12) underwent sham operation and received a 2% cholesterol diet. The naïve group (n = 12) received a regular diet. After 8 weeks, cystometrograms (CMG) without anesthesia or restraint were performed. In bladders from each group, oxidative stress markers (8-hydroxy-2'-deoxyguanosine: 8-OHdG; malondialdehyde: MDA) and proinflammatory cytokines (IL-8 like cytokine CXCL1/CINC-1, TNF-α, IL-6) were quantified. Histological examination of the iliac arteries was also performed.
  
  
  RESULTS
  At 8 weeks, the body and bladder wet weights were not significant different among the three groups. The micturition interval in the AI group decreased significantly compared with those in the other two groups, but maximum pressure during micturition did not change. The iliac arteries in the AI group revealed thickening of intima as well as diffuse media fibrosis at the sites of balloon injury. The levels of oxidative stress markers and proinflammatory cytokines were significantly higher in the AI than in the other groups.
  
  
  CONCLUSIONS
  Oxidative stress and inflammation may be key factors in the development of bladder overactivity in atherosclerosis-induced chronic bladder ischemia.
authors.affiliation: Department of Urology, Fukushima Medical University School of Medicine, Fukushima City, Japan. mnomiya@fmu.ac.jp
authors.forename: Masanori
authors.initials: M
authors.lastname: Nomiya
authors.forename: Koji
authors.initials: K
authors.lastname: Sagawa
authors.forename: Junji
authors.initials: J
authors.lastname: Yazaki
authors.forename: Norio
authors.initials: N
authors.lastname: Takahashi
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Kushida
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Haga
authors.forename: Ken
authors.initials: K
authors.lastname: Aikawa
authors.forename: Takahiro
authors.initials: T
authors.lastname: Matsui
authors.forename: Michiko
authors.initials: M
authors.lastname: Oka
authors.forename: Tomomi
authors.initials: T
authors.lastname: Fukui
authors.forename: Karl-Erik
authors.initials: KE
authors.lastname: Andersson
authors.forename: Osamu
authors.initials: O
authors.lastname: Yamaguchi
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D050197:Atherosclerosis / Q000150:complications* / Q000473:pathology; D015415:Biomarkers / Q000378:metabolism; D002908:Chronic Disease; D016207:Cytokines / Q000378:metabolism*; D003849:Deoxyguanosine / Q000031:analogs & derivatives* / Q000378:metabolism; D004195:Disease Models, Animal; D007083:Iliac Artery / Q000473:pathology; D007511:Ischemia / Q000209:etiology* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015854:Up-Regulation / Q000502:physiology; D001743:Urinary Bladder / Q000098:blood supply*; D053201:Urinary Bladder, Overactive / Q000378:metabolism / Q000503:physiopathology*; D014554:Urination / Q000502:physiology; D014563:Urodynamics / Q000502:physiology
chemical_list: D015415:Biomarkers; D016207:Cytokines; D008315:Malondialdehyde; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine