title: The loss and progressive recovery of voiding after spinal cord interruption in rats is associated with simultaneous changes in autonomous contractile bladder activity.
abstract: BACKGROUND
  Autonomous contractile activity (ACA) is a well-known phenomenon in isolated bladders from different species and seems to be important in the physiology of both normal and dysfunctional voiding.
  
  
  OBJECTIVE
  To determine whether ACA is changed in bladders from paraplegic rats at different periods post-spinal cord injury (post-SCI).
  
  
  METHODS
  ACA was studied in bladders (at least six per group) from normal and paraplegic female Wister rats at different times post-SCI (2 h, 24 h, 1 wk, and 3 wk). A group of normal rats was used as a control group. For measurements bladders were incubated in organ baths under standardised conditions.
  
  
  METHODS
  ACA was measured as pressure change, which was defined as either a transient change or a spiked change according to its characteristics. The effects of intravesical volume load and muscarinic agonists were studied.
  
  
  CONCLUSIONS
  Following spinal cord injury (SCI) a clear evolution in ACA was observed. In bladders from SCI rats in the acute areflexive voiding phase (1 wk post-SCI), we observed decreased ACA associated with a highly increased compliance and a changed response to muscarinic agonists. ACA in bladders from SCI rats with renewed voiding reflexes (3 wk post-SCI) was increased, together with a moderately increased compliance and a (moderately) changed response to muscarinic agonists.
  
  
  CONCLUSIONS
  From these observations it is apparent that SCI leads to alterations in the behaviour and muscarinic response of ACA in the isolated bladder. These changes in ACA may play an important role in the pathophysiology of overactive bladder disease (OAB), and interacting with changed ACA might be promising in the search for newer treatments for OAB.
authors.affiliation: KU Leuven, Department of Urology, University Hospitals Gasthuisberg, Leuven, Belgium. Thomas.gevaert@uz.kuleuven.ac.be
authors.forename: Thomas
authors.initials: T
authors.lastname: Gevaert
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Owsianik
authors.forename: Graham
authors.initials: G
authors.lastname: Hutchings
authors.forename: Liesbeth
authors.initials: L
authors.lastname: Van Leuven
authors.forename: Wouter
authors.initials: W
authors.lastname: Everaerts
authors.forename: Bernd
authors.initials: B
authors.lastname: Nilius
authors.forename: Dirk
authors.initials: D
authors.lastname: De Ridder
mesh_terms: D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D004195:Disease Models, Animal; D005260:Female; D066298:In Vitro Techniques; D018721:Muscarinic Agonists / Q000494:pharmacology; D009119:Muscle Contraction; D009929:Organ Size; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000150:complications* / Q000503:physiopathology*; D001743:Urinary Bladder / Q000473:pathology / Q000503:physiopathology; D053201:Urinary Bladder, Overactive / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology* / Q000652:urine; D014549:Urinary Incontinence / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology* / Q000652:urine
chemical_list: D018721:Muscarinic Agonists; D002217:Carbachol