Comparison of the effects of complete and incomplete spinal cord injury on lower urinary tract function as evaluated in unanesthetized rats

Leung, Paul; Johnson, Christopher; Wrathall, Jean R.

doi:10.1016/j.expneurol.2007.07.013

Cited by 33 publications

(42 citation statements)

References 44 publications

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“…Difference is significant at P ϭ 0.008. allowed for the development of both powerful micturition contractions and phasic EUS-EMG activity, many strong voiding contractions in conscious rats lack phasic EUS-EMG activity. This confirms recent data from Leung et al (23).…”

Section: Substance P Expression In the L6 Spnsupporting

confidence: 83%

Sprouting of substance P-expressing primary afferent central terminals and spinal micturition reflex NK1 receptor dependence after spinal cord injury

Zhang¹,

Douglas²,

Jin³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Dolber PC. Sprouting of substance P-expressing primary afferent central terminals and spinal micturition reflex NK1 receptor dependence after spinal cord injury. Am J Physiol Regul Integr Comp Physiol 295: R2084 -R2096, 2008. First published October 22, 2008 doi:10.1152/ajpregu.90653.2008.-The primary afferent neurotransmitter triggering the spinal micturition reflex after complete spinal cord injury (SCI) in the rat is unknown. Substance P detected immunohistochemically in the sacral parasympathetic nucleus was significantly higher in 12 SCI rats than in 12 spinally intact rats (P ϭ 0.008), suggesting substance P as a plausible candidate for the primary afferent neurotransmitter. The effects of the tachykinin NK1 receptor antagonist L-733060 on the spinal micturition reflex were then determined by performing conscious cystometry in an additional 14 intact rats and 14 SCI rats with L-733060 (0.1-100 g) administered intrathecally at L6-S1. L-733060 was without effect in intact rats, but blocked the spinal micturition reflex in 10 of 14 SCI rats and increased the intermicturition interval in 2 of 4 others at doses ranging from 10 to 100 g. Both phasic and nonphasic voiding contractions, differentiated according to the presence of phasic external urethral sphincter (EUS) activity, were present in most SCI rats. Both types of contractions were blocked by high doses of L-733060. Interestingly, there was a relative decline in phasic voiding contractions at high doses as well as a decline in contraction amplitude in nonphasic voiding contractions. In other respects, cystometric variables were largely unaffected in either spinally intact or SCI rats. L-733060 did not affect tonic EUS activity at any dose except when the spinal micturition reflex was blocked and tonic activity was consequently lost. These experiments show that tachykinin action at spinal NK1 receptors plays a major role in the spinal micturition reflex in SCI rats.spinal cord injury; bladder; tachykinins; external urethral sphincter MICTURITION IN SPINALLY INTACT rats is controlled by a spinobulbospinal reflex (9), in which afferent signals from the bladder are relayed to the pontine micturition center; an afferent-activated neuronal "switch" is thrown when the bladder reaches its capacity for innocuous stretch, and thereafter descending activation of parasympathetic preganglionic neurons in the sacral parasympathetic nucleus (SPN) induces bladder contraction and micturition. Axons of both ascending and descending portions of the reflex pathway are interrupted by spinal cord transection and the spinobulbospinal reflex is lost. However, a purely spinal micturition reflex develops for volume-evoked micturition within ϳ1 wk (47).The neurotransmitters used by primary afferent neurons in the spinal micturition reflex are unknown. In spinally intact rats, the neurotransmitters most likely to be used by bladder primary afferent neurons are neuropeptides and glutamate. Neuropeptides (e.g., substance P, neurokinin A, calcitonin gene-related peptide) are used mo...

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Section: Substance P Expression In the L6 Spnsupporting

confidence: 83%

Sprouting of substance P-expressing primary afferent central terminals and spinal micturition reflex NK1 receptor dependence after spinal cord injury

Zhang¹,

Douglas²,

Jin³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…8 There are various possibilities that might explain the difference between the groups, including the re-establishment of descending circuitry or regeneration of neuromodulatory axons, including serotonergic fibers, as suggested earlier, 18,19 following a contusion injury 13 or a complete lesion. 20 The idea that serotonergic fibers might be involved in the observed maintenance of bladder function is supported by our earlier studies, in which serotonergic fibers, which had originated from the raphe nuclei, were able to regenerate across the cellular bridge and into the spinal cord caudal to the injury. 8 Furthermore, earlier literature showed that the injection of transneuronal tracer (Pseudorabies virus) into the external urethral sphincter or bladder labeled cells in the raphe magnus and raphe pallidus.…”

Section: Discussionmentioning

confidence: 77%

Transplantation and repair: Combined cell implantation and chondroitinase delivery prevents deterioration of bladder function in rats with complete spinal cord injury

et al. 2009

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Methods: Eight rats received Schwann cells in Matrigel-filled guidance channels, olfactory ensheathing glia and chondroitinase ABC at the lesion site following complete thoracic SCI. Controls (n ¼ 7) received Matrigel only. Daily bladder examinations were performed. Analysis of bladder size, wall thickness, actin and collagen type III was performed after 14 weeks. Results: Following SCI, both groups regained bladder voiding after 3 weeks. However, 2 weeks later, incontinence was observed in all untreated rats and two treated rats. Post-mortem examination of bladders revealed enlarged bladder sizes. Thicker bladder walls were found in untreated rats, which were composed of disorganized bundles of smooth muscle fibers surrounded by high amounts of collagen (type III). Conclusion: We show that the combined treatment prevents collagen deposition in bladder walls and maintains the rat's ability to void efficiently. Although the mechanism responsible for this improvement is unclear, our study shows that the present combinatory therapy can influence bladder function, thus expanding their utility as a broad reparative approach for SCI.

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“…Several theories have been proposed for this variability in recovery of bladder function after SCI. Some groups propose that differences in local neurotrophic factors may alter sprouting of primary afferent neurons, which influences bladder functional outcomes; others suggest that the timing and nature of the inflammatory reaction resulting from SCI may alter bladder function (14,(27)(28)(29)(30). While this variability adds complexity to our model, it makes our model more applicable to the human disease state, in which there is noticeable diversity in the degree of bladder dysfunction among SCI and spina bifida patients.…”

Section: Discussionmentioning

confidence: 93%

“…This was initially surprising given that all surgeries performed were complete transections of the spinal cord at the same thoracic cord level by the same surgeon. However, the wide variation in residual volumes has been reported by others (14,27). Several theories have been proposed for this variability in recovery of bladder function after SCI.…”

Section: Discussionmentioning

confidence: 97%

Enhanced Susceptibility to Urinary Tract Infection in the Spinal Cord-Injured Host with Neurogenic Bladder

et al. 2013

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g Neurogenic bladder predisposes to recurrent urinary tract infections (UTI) and renal failure, and susceptibility is commonly ascribed to urinary stasis from elevated residual urine volumes. Escherichia coli UTI was modeled in the spinal cord-injured (SCI) rat with the hypothesis that SCI animals would require fewer bacteria to establish infection, have an exaggerated inflammatory response, and have delayed clearance of infection compared to normal-voiding controls. T10 SCI rats and controls had median infectious doses (ID 50 ) of 10 2 and 10 5 CFU, respectively. Mean residual volumes in the SCI animals did not correlate with susceptibility to initiation of UTI or outcome. In the acute infection, control and SCI rats developed acute cystitis and pyelitis without acute differences in histopathological scores of inflammation. However, in vivo imaging of infected animals revealed persistently higher levels of bacteria in the SCI urine and bladders than were seen for controls over 2 weeks. Likewise, at 2 weeks, acute and chronic inflammatory infiltrates persisted in the bladders and kidneys of SCI rats, whereas inflammation largely resolved within the controls. Together these data demonstrate that SCI rats exhibit delayed clearance of infection and exaggerated inflammatory responses in bladders and kidneys; however, the severity of residual volumes does not predict increased susceptibility to UTI. These studies suggest that host-dependent mechanisms that are discrete from alterations in bladder physiology influence UTI susceptibility with the SCI-neurogenic bladder. This model will allow elucidation of SCI-neurogenic bladder-mediated changes in host response that yield UTI susceptibility and may lead to new preventative and therapeutic options. N eurogenic bladder refers to bladder dysfunction that is secondary to disruption of the central or peripheral nervous system pathways that regulate bladder storage and emptying. In children, the most common causes of neurogenic bladder are neural tube defects, such as spina bifida (myelomeningocele), while in adults, the most common cause is trauma-related spinal cord injury (SCI). Regardless of etiology, all patients with neurogenic bladder are at significantly increased risk for recurrent urinary tract infections (UTI) compared to the normally voiding population, with an annual incidence as high as 20 to 25% (1).A number of risk factors have been postulated for the increased susceptibility to UTI in patients with neurogenic bladder. They include urinary stasis due to elevated postvoid residual volumes, bladder overdistention, high-pressure voiding, vesicoureteral reflux, nephrolithiasis, and the use of chronic indwelling catheters. Many patients with neurogenic bladder perform scheduled clean intermittent catheterizations (CIC) to assist with bladder emptying. However, these individuals still have a 4-fold-increased risk of UTI compared to those who do not perform CIC (2, 3). Given the frequency of UTI, many neurogenic bladder patients are exposed to repeated courses of t...

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Comparison of the effects of complete and incomplete spinal cord injury on lower urinary tract function as evaluated in unanesthetized rats

Cited by 33 publications

References 44 publications

Sprouting of substance P-expressing primary afferent central terminals and spinal micturition reflex NK1 receptor dependence after spinal cord injury

Sprouting of substance P-expressing primary afferent central terminals and spinal micturition reflex NK1 receptor dependence after spinal cord injury

Transplantation and repair: Combined cell implantation and chondroitinase delivery prevents deterioration of bladder function in rats with complete spinal cord injury

Enhanced Susceptibility to Urinary Tract Infection in the Spinal Cord-Injured Host with Neurogenic Bladder

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