title: The potential of hormones and selective oestrogen receptor modulators in preventing voiding dysfunction in rats.
abstract: OBJECTIVE
  To investigate whether oestrogen, selective oestrogen receptor modulators (SERMs), and growth hormone (GH) can prevent the development of voiding dysfunction in a postpartum postmenopausal rat model of voiding dysfunction.
  
  
  METHODS
  Immediately after spontaneous delivery, nine primiparous Sprague-Dawley rats served as uninjured controls (sham group) and 54 underwent intravaginal balloon dilation. On day 7, the 54 subject rats underwent bilateral ovariectomy. A week later, six treatment groups of nine rats were randomized to receive: normal saline (injured control group), 17beta-oestradiol (E(2)), raloxifene, levormeloxifene, GH, or GH + E(2). The treatment groups received daily subcutaneous injections for 3 weeks. The effects of hormone treatment were examined by conscious cystometry at the end of the study. Voiding dysfunction was defined to include overactive bladder and sphincter deficiency.
  
  
  RESULTS
  The sham rats had a mean (sd) voiding frequency of 3 (0.87) times in 10 min and a bladder capacity of 0.43 (0.13) mL with smooth cystometry curves. The number of rats in each treatment group (each group contained nine rats) that had voiding dysfunction was as follows: E(2), three; raloxifene, six; levormeloxifene, four; and controls, four (P > 0.05 among the groups). Only one rat in the GH-treated group and no rats in the GH + E(2)-treated group had voiding dysfunction, which was significantly less in the GH + E(2)-treated group than in the controls (P = 0.041).
  
  
  CONCLUSIONS
  This functional data suggest that the development of voiding dysfunction can be prevented by short-term administration of GH and GH + E(2) in our rat model. SERMs and E(2) alone seem to have no therapeutic effect.
authors.affiliation: Knuppe Molecular Urology Laboratory, Department of Urology, University of California-San Francisco, San Francisco, CA 94143-0738, USA.
authors.forename: Kavirach
authors.initials: K
authors.lastname: Tantiwongse
authors.forename: Thomas M
authors.initials: TM
authors.lastname: Fandel
authors.forename: Guifang
authors.initials: G
authors.lastname: Wang
authors.forename: Benjamin N
authors.initials: BN
authors.lastname: Breyer
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Walsh
authors.forename: Anthony J
authors.initials: AJ
authors.lastname: Bella
authors.forename: Tom F
authors.initials: TF
authors.lastname: Lue
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D004195:Disease Models, Animal; D004359:Drug Therapy, Combination; D004967:Estrogens / Q000627:therapeutic use*; D005260:Female; D013006:Growth Hormone / Q000627:therapeutic use*; D007748:Labor Stage, Second / Q000502:physiology; D007744:Obstetric Labor Complications / Q000503:physiopathology*; D010865:Pilot Projects; D017698:Postmenopause / Q000502:physiology; D011247:Pregnancy; D011644:Puerperal Disorders / Q000517:prevention & control; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D020845:Selective Estrogen Receptor Modulators / Q000627:therapeutic use*; D053201:Urinary Bladder, Overactive / Q000517:prevention & control*; D014549:Urinary Incontinence / Q000517:prevention & control*; D014563:Urodynamics / Q000502:physiology
chemical_list: D004967:Estrogens; D020845:Selective Estrogen Receptor Modulators; D013006:Growth Hormone