title: Time dependent changes in diabetic cystopathy in rats include compensated and decompensated bladder function.
abstract: OBJECTIVE
  Diabetic bladder dysfunction is among the most common and bothersome complications of diabetes mellitus. While bladder filling and voiding problems have been reported, the precise functional changes in diabetic bladders remain unclear. We investigated time dependent changes in bladder function in streptozotocin induced diabetic rats.
  
  
  METHODS
  Cystometrograms and detrusor muscle contractility were examined in male age matched control and diabetic Sprague-Dawley rats (Harlan, Indianapolis, Indiana) 3, 6, 9, 12 and 20 weeks after diabetes induction with streptozotocin.
  
  
  RESULTS
  Diabetes decreased average body weight and increased bladder weight, capacity and compliance. Peak detrusor leak pressure increased gradually from weeks 3 to 6 to 9 in diabetic rats (mean +/- SEM 47.3 +/- 2.5, 50.8 +/- 3.0 and 56.0 +/- 3.6 cm H(2)O) and in controls (36.9 +/- 1.4, 37.7 +/- 1.5 and 41.6 +/- 1.81 cm H(2)O, respectively). However, at 12 and 20 weeks diabetic rats deviated strongly from this trend with peak detrusor leak pressure decreasing vs controls (41.6 +/- 2.8 and 37.3 +/- 0.9 vs 45.2 +/- 1.7 and 49.6 +/- 1.4 cm H(2)O, respectively) and post-void resting pressures increasing from 9-week levels vs controls (interactions p <0.0001). In contractility studies increased contractile force responses of diabetic animals to carbamylcholine chloride, potassium chloride, adenosine 5'-triphosphate and electric field stimulation peaked at 6 or 9 weeks but at 12 to 20 weeks they generally reverted toward those of controls (carbamylcholine chloride and electrical field stimulation interactions p = 0.0022 and 0.01, respectively).
  
  
  CONCLUSIONS
  Diabetic bladders may undergo a transition from a compensated to a decompensated state and transition in the streptozotocin rat model may begin 9 to 12 weeks after induction.
authors.affiliation: Glickman Urological Institute, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA. daneshf@ccf.org
authors.forename: Firouz
authors.initials: F
authors.lastname: Daneshgari
authors.forename: Guiming
authors.initials: G
authors.lastname: Liu
authors.forename: Peter B
authors.initials: PB
authors.lastname: Imrey
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D048909:Diabetes Complications / Q000473:pathology / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D004558:Electric Stimulation; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D001743:Urinary Bladder / Q000473:pathology / Q000503:physiopathology*; D001750:Urinary Bladder, Neurogenic / Q000473:pathology / Q000503:physiopathology; D014549:Urinary Incontinence / Q000473:pathology / Q000503:physiopathology; D014563:Urodynamics
chemical_list: D001786:Blood Glucose