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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Urological research 20 (1992), S. 59-62 
    ISSN: 1434-0879
    Keywords: Urinary bladder ; Overdistension ; Cholinergic Hypoinnervation ; Acetylcholinesterase ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of short-term urinary bladder distension on its cholinergic innervation was studied in Sprague-Dawley rats. Distension was induced for 3 h by forced diuresis and balloon outlet obstruction, and whole thick biopsy specimens were taken from the dome and lateral side of the anterior body 2, 7 and 21 days afterwards. The acetylcholinesterase (AChE) method was used to demonstrate the cholinergic nerves in the distended bladder wall. Cholinergic hypoinnervation was observed 7 days after the distension, persisting up to 21 days, although AChE-reactive nerves were then observed to be more numerous. The distribution of hypoinnervation was uneven, being more marked in the lateral side of the anterior body than in the dome. The distribution of AChE-reactive nerves varied even in the same biopsies, with areas of total hypoinnervation occurring next to areas of slightly diminished innervation. This was especially true 21 days after cholinergic innervation, which may in turn explain the prolonged voiding difficulties often seen after catheterization of an overdistended bladder in a patient with urinary retention. The short-lasting effect of bladder dilatation therapy used to treat detrusor instability or interstitial cystitis may be due to the fairly rapid regeneration of cholinergic innervation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Urological research 18 (1990), S. 345-348 
    ISSN: 1434-0879
    Keywords: Urinary bladder ; Overdistension ; Adrenergic innervation ; SIF cells ; Glyoxylic acid ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of distension on adrenergic innervation was investigated in the rat urinary bladder. Bladders were distended for 3 h by forced diuresis and ballon obstruction, and specimens were taken from the bladder dome, body and neck for the demonstration of glyoxylic acid-induced fluorescence of catecholamines. Depletion of catecholamines started after 10 h and was almost complete after 2 days. The fluorescence had recovered part way after 5–7 days and was practically normal after 21 days. Small, intensely fluorescent (SIF) cells in the ganglia continued to leak catecholamines throughout the 21-day study period. The primary clinical success of distension therapy for the treatment of unstable bladder may be at least partly due to a reversible disturbance in the function of the adrenergic nerves, which have an excitatory alpha-adrenergic dominance in such cases, but the persistent leakage from SIF cells raises the question of whether distension causes prolonged disturbances in bladder function.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1434-0879
    Keywords: Neuropeptide Y ; Vasoactive intestinal polypeptide ; Substance P ; Bladder distension ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of acute distension on vasoactive polypeptide (VIP)-, neuropeptide Y (NPY)- and substance P (SP)-immunoreactive nerves in the wall of the urinary bladder was investigated. At the age of 3 months, 25 female albino rats underwent forced diuresis combined with balloon obstruction to achieve maximal distension for 3 h. A modified, indirect immunofluorescence detection method was applied 2 days, 7 days and 21 days after distension. A marked, extensive depletion of VIP, NPY-and SP-immunoreactive nerves was observed after distension. This disturbance was reversible, and increased fluorescence of VIP-, NPY- and SP-immunoreactive nerve fibres compared with control specimens was seen in bladder specimens taken even as soon as 21 days after distension. This transient depletion of peptidergic innervation may partly explain the prolonged voiding problems that often occur after acute urinary retention. The depletion of sensory nerves containing SP shortly after distension may explain the transient benefit obtained from distension therapy in patients with painful bladder disease. It is suggested that the increased SP activity during the recovery phase may be related to neurogenic inflammation.
    Type of Medium: Electronic Resource
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