Diabetic Cystopathy:
Neuropathological Examination of Urinary Bladder Biopsies

Poppel, Hein Van; Stessens, R.; Damme, Boudewijn Van; Carton, Herwig; Baert, Luc

doi:10.1159/000473412

Cited by 42 publications

(24 citation statements)

References 17 publications

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“…In diabetes a majority of the samples showed lower AChE and increased SI00 density compatible with dia betic neuropathy as reported previously [Van Poppel et al, 1988b]. In all these patients, with urodynamically proven underactive detrusor function, VIP was de creased.…”

Section: Discussionsupporting

confidence: 82%

“…Increased SI00 density re flects Schwann cell hyperplasia occurring in MS as a regeneration attempt after neurogenic damage, indicat ing that MS is not a disease limited to the central ner vous system but also affects the peripheral nervous sys tem [Gu et al, 1984d;Van Poppel et al, 1988a], The significance of decreased SI00 is still uncertain [Van Poppel et al, 1988a], For VIP we only found decreased immunoreactivity in about 50% of the MS patients pre senting with urodynamically proven detrusor hyperreflexia. VIP was slightly decreased in 11 patients and markedly decreased in 4 of them.…”

Section: Discussionmentioning

confidence: 86%

See 1 more Smart Citation

Vasoactive Intestinal Polypeptidergic Innervation of Human Urinary Bladder in Normal and Pathological Conditions (With 1 color plate)

Poppel¹,

Stessens²,

Baert³

et al. 1988

Urol Int

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Urinary bladder biopsies from 31 multiple sclerosis patients, 9 diabetics, 5 patients after transtrigonal phenolization and 20 control patients were stained for acetylcholinesterase, S100 and vasoactive intestinal polypeptide (VIP). The VIP immunoreactivity was not decreased in all neuropathic bladders and its depletion was not related to cholinergic depletion. There was no correlation between bladder over- or underactivity and VIP content. VIP can act as a modulator of detrusor function in normal conditions. The significance of its depletion in neurogenic bladders needs further elaboration.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 86%

Vasoactive Intestinal Polypeptidergic Innervation of Human Urinary Bladder in Normal and Pathological Conditions (With 1 color plate)

Poppel¹,

Stessens²,

Baert³

et al. 1988

Urol Int

Self Cite

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“…The neuropathies of DM caused by the metabolic derangement of the Schwann cell result in segmental demyelination and impairment of nerve conduction (404,459,658). Some of the proposals for pathogenesis of DM neuropathy include altered metabolism of glucose, ischemia, superoxide-induced freeradical formation and impaired axonal transport (22).…”

Section: Diabetes Mellitus and Detrusor Underactivitymentioning

confidence: 99%

Neural Control of the Lower Urinary Tract

1997

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This article summarizes anatomical, neurophysiological, pharmacological, and brain imaging studies in humans and animals that have provided insights into the neural circuitry and neurotransmitter mechanisms controlling the lower urinary tract. The functions of the lower urinary tract to store and periodically eliminate urine are regulated by a complex neural control system in the brain, spinal cord, and peripheral autonomic ganglia that coordinates the activity of smooth and striated muscles of the bladder and urethral outlet. The neural control of micturition is organized as a hierarchical system in which spinal storage mechanisms are in turn regulated by circuitry in the rostral brain stem that initiates reflex voiding. Input from the forebrain triggers voluntary voiding by modulating the brain stem circuitry. Many neural circuits controlling the lower urinary tract exhibit switch-like patterns of activity that turn on and off in an all-or-none manner. The major component of the micturition switching circuit is a spinobulbospinal parasympathetic reflex pathway that has essential connections in the periaqueductal gray and pontine micturition center. A computer model of this circuit that mimics the switching functions of the bladder and urethra at the onset of micturition is described. Micturition occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary micturition, leading to urinary incontinence. Neuroplasticity underlying these developmental and pathological changes in voiding function is discussed.

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“…It has been suggested that urinary bladder dysfunction in chronic diabetes might be due to an altered response of the organ to autonomic stimuli (Kamata et al, 1992). Segmental demyelination and axonal degeneration of the peripheral autonomic nerves have also been reported to cause dysfunction of lower urinary bladder tract (van Poppel et al, 1988). Several studies have been undertaken to investigate contractile responses of the bladder to muscarinic drugs in diabetic animals.…”

Section: Introductionmentioning

confidence: 99%

Diabetes mellitus and responses of the urinary bladder to acetylcholine: an in vitro study

Nsabimana

Ojewole

2008

J. Smooth Muscle Res.

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This study was prompted by the inconsistent reports and apparent controversies that exist in the biomedical literature on the responses of diabetic bladder strips to cholinergic nerve stimulation or exogenously-administered muscarinic agonists, especially acetylcholine (ACh). In the present study, acetylcholine-induced contractions of urinary bladders isolated from normoglycaemic (normal) and streptozotocin-treated, diabetic Wistar rats were examined under physiological conditions. Mechanical contractile changes of the isolated urinary bladders of STZ-treated, diabetic rats in response to bath-applied acetylcholine were compared with those obtained from isolated urinary bladders of normal, age-matched, control rats. Results obtained show that urinary bladders from diabetic rats were always more spontaneously active after mounting, than those of the age-matched normal, control rats. ACh (10 -8 -10 -4 M) provoked concentration-related, atropine-sensitive contractions of the isolated urinary bladders of both diabetic and age-matched normal, control rats. However, acetylcholine always induced more powerful and greater contractions of the diabetic bladders compared with bladders from the age-matched normal, control rats. The magnitude and/ or intensity of the diabetic bladder enhanced contractile responses to ACh continued to increase as the diabetic state of the animals progressed.

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Diabetic Cystopathy: Neuropathological Examination of Urinary Bladder Biopsies

Cited by 42 publications

References 17 publications

Vasoactive Intestinal Polypeptidergic Innervation of Human Urinary Bladder in Normal and Pathological Conditions (With 1 color plate)

Vasoactive Intestinal Polypeptidergic Innervation of Human Urinary Bladder in Normal and Pathological Conditions (With 1 color plate)

Neural Control of the Lower Urinary Tract

Diabetes mellitus and responses of the urinary bladder to acetylcholine: an in vitro study

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