The development of reflex bladder activity following spinal cord injury in cats and a method to control it

McGuire, Edward J.; Morrissey, Susan G.

doi:10.1002/nau.1930010214

Cited by 17 publications

(2 citation statements)

References 9 publications

(7 reference statements)

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“…Phasic bursting EUS EMG activity has also been seen in other animals, including dogs [ 139 , 187 ] and some nonhuman primates [ 206 , 207 ]. However, EUS EMG activity is silenced during micturition in humans, pigs [ 31 ] and felines [ 208 , 209 , 210 ]; therefore, intravesical pressure oscillations with concomitant urethral sphincter activation indicates the presence of DSD after SCI. The fact that this potentially pathologic pattern of bladder and EUS activation in humans is a feature of normal voiding in mice, rats, dogs and NHPs complicates the use of these animal models for studying DSD; nonetheless, since the pattern of EUS EMG activation in DSD is significantly different from that of phasic bursting during voiding, it remains viable to use rodents for neurogenic bladder investigations with this understanding.…”

Section: Considerations For the Application Of Animal Models In Nlutd...mentioning

confidence: 99%

Assessing Neurogenic Lower Urinary Tract Dysfunction after Spinal Cord Injury: Animal Models in Preclinical Neuro-Urology Research

et al. 2023

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Neurogenic bladder dysfunction is a condition that affects both bladder storage and voiding function and remains one of the leading causes of morbidity after spinal cord injury (SCI). The vast majority of individuals with severe SCI develop neurogenic lower urinary tract dysfunction (NLUTD), with symptoms ranging from neurogenic detrusor overactivity, detrusor sphincter dyssynergia, or sphincter underactivity depending on the location and extent of the spinal lesion. Animal models are critical to our fundamental understanding of lower urinary tract function and its dysfunction after SCI, in addition to providing a platform for the assessment of potential therapies. Given the need to develop and evaluate novel assessment tools, as well as therapeutic approaches in animal models of SCI prior to human translation, urodynamics assessment techniques have been implemented to measure NLUTD function in a variety of animals, including rats, mice, cats, dogs and pigs. In this narrative review, we summarize the literature on the use of animal models for cystometry testing in the assessment of SCI-related NLUTD. We also discuss the advantages and disadvantages of various animal models, and opportunities for future research.

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Section: Considerations For the Application Of Animal Models In Nlutd...mentioning

confidence: 99%

Assessing Neurogenic Lower Urinary Tract Dysfunction after Spinal Cord Injury: Animal Models in Preclinical Neuro-Urology Research

et al. 2023

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“…Vesical hypertonicity following lower-motor neuron lesions has traditionally been explained by detrusor supersensitivity to cholinergic agonists [Lapides, 1962;El-Salmy et al, 19851 and/or detrusor hypertrophy in the face of a fixed urethral closure pressure [McGuire et al, 1981;McGuire and Morrissey, 1982;McGuire, 19861. Our observations in the present study suggest that yet another factor may contribute to the development of hypertonicity in the lower-motor neurogenic bladder. It has been reported that postdecentralization adrenergic hyperinnervation of the detrusor is accompanied by exaggerated a-adrenergic responses; this was suggested as a factor in the development of hypertonicity in the decentralized bladder [Sundin and Dahlstrom, 1973;Sundin et al, 19771.…”

Section: Clinicomorphologic Correlationmentioning

confidence: 99%

Intrinsic neuromuscular defects in the neurogenic bladder: IX. Effects of combined parasympathetic decentralization and hypogastric neurectomy on neuromuscular ultrastructure of the feline bladder base

Hanno

Atta

Elbadawi

1988

Neurourology and Urodynamics

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Previous studies have shown that unilateral decentralization of the feline bladder by sacral ventral rhizotomy results in ultrastructural neuromuscular changes in the bladder base. In the present study, the neuromuscular ultrastructure of the feline bladder base was studied in twenty sexually mature adult male cats 1-4 and 6-10 weeks following bilateral sacral rhizotomy, alone and combined with hypogastric neurectomy. The former procedure resulted in initial degeneration of cholinergic axons with loss of their neuroeffector junctions, but the adrenergic axons and neuroeffector junctions were preserved; within 6-10 weeks, the bladder base became re-innervated by regenerated cholinergic, increased adrenergic, and abundant probable copeptidergic axons. In contrast, combined sacral rhizotomy and hypogastric neurectomy resulted in persistent (up to 10 weeks) degeneration of both cholinergic and adrenergic axons with loss of their neuroeffector junctions, and no adrenergic hyperinnervation, with only a modest increase in probable copeptidergic axons in long-term samples. Our observations indicate that intact efferent sympathetic pathways are essential for eventual cholinergic re-innervation and adrenergic hyperinnervation of the decentralized bladder and suggest that the latter is an important factor in the development of vesical hypertonicity in lower-motor neuron lesions. On this basis, we introduce the concept that two functional types of the lower motor neurogenic bladder-i.e., the Received for publication October 19, 1987; accepted February 11, 1988. hypertonic with intact and the normotonic with injured efferent sympathetic pathwaysmay be distinguishable morphologically by ultrastructural study of the vesical muscularis.

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Micturitional Reflexes in Chronic Spinalized Cats: The Underactive Detrusor and Detrusor‐Sphincter Dyssynergia

Galeano

Jubelin

Germain

et al. 1986

Neurourology and Urodynamics

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We studied micturitional reflexes in 46 unanesthetized adult male cats spinalized at C5-C6 17 to 125 days previously and in eight intact central nervous system chloralosed cats that were used as controls. Urethral pressure profiles, cystosphincterograms with the urethrovesical junction opened and closed, and mechanograms of detrusor and circular and longitudinal urethral muscles were performed. The effect of vesical, urethral, pelvic, or pudendal anesthesia and vesical and urethral mechanical stimulation were studied. Our results suggest that spinalization produces two major types of neurourologic disorders: (1) weakness of detrusor contractor reflexes (vesicovesical and urethrovesical contraction reflexes) and (2) exaggeration of urethral contractor reflexes (urethrourethral contraction reflex, guarding reflex). Secondarily the weakness of detrusor contractions diminishes the efficiency of the urethral reflex relaxation needed for voiding (vesicourethral relaxation reflex). Because of these abnormalities, two main syndromes appear: (1) underactive detrusor function and (2) detrusor sphincter dyssynergia. Isolated peripheral manipulations of the bladder or urethra do not improve micturition: (1) increase in detrusor contraction strength induces detrusor sphincter dyssynergia, and (2) relaxation of the external sphincter facilitates voiding, but urinary retention persists. It is proposed that spinalization produces a central micturitional dysreflexia responsible for the peripheral dysfunction, and treatment must be oriented toward the central dysreflexia rather than the peripheral dysfunction.

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The development of reflex bladder activity following spinal cord injury in cats and a method to control it

Cited by 17 publications

References 9 publications

Assessing Neurogenic Lower Urinary Tract Dysfunction after Spinal Cord Injury: Animal Models in Preclinical Neuro-Urology Research

Assessing Neurogenic Lower Urinary Tract Dysfunction after Spinal Cord Injury: Animal Models in Preclinical Neuro-Urology Research

Intrinsic neuromuscular defects in the neurogenic bladder: IX. Effects of combined parasympathetic decentralization and hypogastric neurectomy on neuromuscular ultrastructure of the feline bladder base

Micturitional Reflexes in Chronic Spinalized Cats: The Underactive Detrusor and Detrusor‐Sphincter Dyssynergia

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