title: Urinary bladder response to hypogastric nerve stimulation after bilateral resection of the pelvic nerve or spinal cord injury in rats.
abstract: BACKGROUND
  We examined the mechanism of urinary bladder motility return after bladder areflexia induced by interruption of the sacral parasympathetic outflow to the urinary bladder following damage to the sacral cord or pelvic nerves in the rat.
  
  
  METHODS
  The L6 and S1 nerve bundles were resected near the vertebrae, and bilateral pelvic nerve resections (PNR) performed. Spinal cord injury (SCI) was performed by means of a legion generator at the T12 vertebra. Thirty days after PNR and SCI, cystometrograms were recorded under anesthesia.
  
  
  RESULTS
  In all rats subjected to PNR or SCI, overflow incontinence continued, yet some rats subjected to SCI recovered within 2 weeks after the operation. Cystometrograms showed that repetitive bladder contractions appeared in rats subjected to SCI irrespective of hypogastric nerve (HGN) innervation, while bladder contractions did not appear in rats subjected to PNR. Electrical stimulation of the HGN induced higher bladder pressure elevation in rats who underwent PNR than in rats subjected to SCI.
  
  
  CONCLUSIONS
  These results suggest that the generation of repetitive bladder contractions induced by bladder distention after bladder areflexia requires the presence of intact pelvic nerves that transmit sacral cord-originating excitatory information to the bladder. However, the HGN system and functioning pelvic nerve ganglia are not involved in this process. Also, the connection from the preganglionic HGN to the postganglionic parasympathetic nerves in the pelvic plexus did not form after PNR.
authors.affiliation: Department of Pharmacology, Faculty of Pharmaceutical Science, Hokuriku University, Kanagawa, Kanazawa, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kontani
authors.forename: K
authors.initials: K
authors.lastname: Hayashi
mesh_terms: D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002908:Chronic Disease; D004558:Electric Stimulation; D018738:Hexamethonium / Q000494:pharmacology; D007001:Hypogastric Plexus / Q000502:physiology* / Q000601:surgery*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D010276:Parasympatholytics / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D011312:Pressure; D051381:Rats; D012018:Reflex / Q000502:physiology; D013119:Spinal Cord Injuries / Q000150:complications / Q000503:physiopathology*; D013565:Sympatholytics / Q000494:pharmacology; D001743:Urinary Bladder / Q000187:drug effects / Q000294:innervation* / Q000502:physiology; D014549:Urinary Incontinence / Q000209:etiology / Q000503:physiopathology; D014563:Urodynamics / Q000187:drug effects / Q000502:physiology
chemical_list: D018733:Nicotinic Antagonists; D010276:Parasympatholytics; D013565:Sympatholytics; D018738:Hexamethonium; D001285:Atropine; D011224:Prazosin; D010646:Phentolamine