title: [Effects of ischemia on voiding function and nerve growth factor of the rat urinary bladder].
abstract: OBJECTIVE
  Nerve growth factor (NGF) is synthesized in the target organs innervated by autonomic and sensory nerves so as to grow, maintain and/or repair the neurons. The present study evaluated the effects of ischemia on NGF synthesis and voiding function of the rat urinary bladder.
  
  
  METHODS
  Bladder ischemia was induced by ligating of bilateral internal iliac arteries in the female rats. We examined the changes in the blood flow, histological structure, voiding function and NGF content of the bladder immediately, 1, 7, 14 and 28 days after the surgery. Blood flow was estimated by measuring absorbance of homogenized bladder tissue after dye injection into the abdominal aorta. Voiding function was assessed by continuous cystometry under an awake restrained condition. NGF was quantified by enzyme immunoassay (ELISA method).
  
  
  RESULTS
  Blood flow decreased to 18% of the control immediately after the vascular ligation, and gradually recovered to 66% of the control on day 28. Histologically, epithelial ablation and thinning of muscle layer were observed on days 1 and 7. These histological disorders gradually improved to normal appearance on day 14. On day 1, while the maximum contraction pressure significantly decreased, the contraction frequency and small prevoiding contraction increased. On the other hand, the voiding efficacy markedly decreased on day 7. These functional changes recovered nearly to the control levels after day 14. NGF content transiently increased 2.4 times as the control on day 1.
  
  
  CONCLUSIONS
  The present results will indicate that the voiding function deteriorated by acute ischemia is temporarily compensated by detrusor hyperrefrexia, which may be attributable to an enhanced NGF synthesis, and then improves by the development of collateral blood circulation.
authors.affiliation: Department of Urology, Akita University School of Medicine.
authors.forename: T
authors.initials: T
authors.lastname: Ishida
authors.forename: N
authors.initials: N
authors.lastname: Shimoda
authors.forename: K
authors.initials: K
authors.lastname: Sato
authors.forename: O
authors.initials: O
authors.lastname: Ogawa
authors.forename: O
authors.initials: O
authors.lastname: Nishizawa
authors.forename: T
authors.initials: T
authors.lastname: Kato
mesh_terms: D000208:Acute Disease; D000818:Animals; D005260:Female; D007511:Ischemia / Q000378:metabolism / Q000503:physiopathology*; D009414:Nerve Growth Factors / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar; D001743:Urinary Bladder / Q000098:blood supply* / Q000378:metabolism / Q000503:physiopathology; D014554:Urination
chemical_list: D009414:Nerve Growth Factors