Effects of Sacral Neuromodulation on Isolated Urinary Bladder Function in a Rat Model of Spinal Cord Injury

2014 ◽  
Vol 18 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Şükrü Kumsar ◽  
Ulya Keskin ◽  
Alaaddin Akay ◽  
Uğur Taylan Bilgilisoy ◽  
Ş. Remzi Erdem ◽  
...  
2019 ◽  
Vol 39 (2) ◽  
pp. 586-593 ◽  
Author(s):  
Elena E. Keller ◽  
Irina Patras ◽  
Ioan Hutu ◽  
Karin Roider ◽  
Karl‐Dietrich Sievert ◽  
...  

Author(s):  
Silvia Wognum ◽  
Michael S. Sacks

Spinal cord injury (SCI) is accompanied by urologic complications, characterized by two phases (early areflexic phase and late hyperreflexic phase), where the routine function of the urinary bladder of storing urine and voiding becomes compromised. In addition to functional deficiencies, these pathologies are often accompanied by changes in bladder wall tissue morphology and mechanical properties. Our experimental studies have revealed that the bladder wall can undergo rapid remodeling post-SCI (figs.1,2) and exhibits complex biomechanical responses (fig.2B) [1,2,3,4]. These remodeling events will result in profound changes in bladder wall biomechanical behavior (fig.2) and ultimately organ function. The specific alterations in mechanical behavior and functional properties of bladder wall tissue and the underlying mechanisms are not well understood. A multi-phase structural constitutive model of the bladder wall is clearly needed to understand how changes in various tissue components produce observed changes in bladder function.


2003 ◽  
Vol 284 (5) ◽  
pp. F966-F976 ◽  
Author(s):  
Gerard Apodaca ◽  
Susanna Kiss ◽  
Wily Ruiz ◽  
Susan Meyers ◽  
Mark Zeidel ◽  
...  

Neural-epithelial interactions are hypothesized to play an important role in bladder function. We determined whether spinal cord injury (SCI) altered several indicators of urinary bladder epithelium barrier function, including continuity of the surface umbrella cell layer, transepithelial resistance (TER), and urea and water permeability. Within 2 h of SCI, significant changes in uroepithelium were noted, including disruption of the surface umbrella cells and an ∼50% decrease in TER. By 24 h, TER reached a minimum and was accompanied by significant increases in water and urea permeability. Regeneration of the surface uroepithelium was accomplished by 14 days after SCI and was accompanied by a return to normal TER and urea and water permeabilities. This early disruption of the uroepithelial permeability and accompanying changes in uroepithelial morphology were prevented by pretreatment with hexamethonium (a blocker of ganglion transmission), indicating involvement of sympathetic or parasympathetic input to the urinary bladder. In addition, prior treatment with capsaicin worsened the effect of SCI on uroepithelial permeability, suggesting that capsaicin-sensitive afferents may play a protective role in the process. These results demonstrate that SCI results in a significant disruption of the urinary bladder uroepithelium and that these changes may be mediated in part by an interaction with bladder nerves.


2021 ◽  
pp. 1-8
Author(s):  
Florence R. A. Hogg ◽  
Siobhan Kearney ◽  
Eskinder Solomon ◽  
Mathew J. Gallagher ◽  
Argyro Zoumprouli ◽  
...  

OBJECTIVE The authors sought to investigate the effect of acute, severe traumatic spinal cord injury on the urinary bladder and the hypothesis that increasing the spinal cord perfusion pressure improves bladder function. METHODS In 13 adults with traumatic spinal cord injury (American Spinal Injury Association Impairment Scale grades A–C), a pressure probe and a microdialysis catheter were placed intradurally at the injury site. We varied the spinal cord perfusion pressure and performed filling cystometry. Patients were followed up for 12 months on average. RESULTS The 13 patients had 63 fill cycles; 38 cycles had unfavorable urodynamics, i.e., dangerously low compliance (< 20 mL/cmH2O), detrusor overactivity, or dangerously high end-fill pressure (> 40 cmH2O). Unfavorable urodynamics correlated with periods of injury site hypoperfusion (spinal cord perfusion pressure < 60 mm Hg), hyperperfusion (spinal cord perfusion pressure > 100 mm Hg), tissue glucose < 3 mM, and tissue lactate to pyruvate ratio > 30. Increasing spinal cord perfusion pressure from 67.0 ± 2.3 mm Hg (average ± SE) to 92.1 ± 3.0 mm Hg significantly reduced, from 534 to 365 mL, the median bladder volume at which the desire to void was first experienced. All patients with dangerously low average initial bladder compliance (< 20 mL/cmH2O) maintained low compliance at follow-up, whereas all patients with high average initial bladder compliance (> 100 mL/cmH2O) maintained high compliance at follow-up. CONCLUSIONS We conclude that unfavorable urodynamics develop within days of traumatic spinal cord injury, thus challenging the prevailing notion that the detrusor is initially acontractile. Urodynamic studies performed acutely identify patients with dangerously low bladder compliance likely to benefit from early intervention. At this early stage, bladder function is dynamic and is influenced by fluctuations in the physiology and metabolism at the injury site; therefore, optimizing spinal cord perfusion is likely to improve urological outcome in patients with acute severe traumatic spinal cord injury.


2012 ◽  
Vol 187 (4S) ◽  
Author(s):  
Dong Han ◽  
Moon Young Lee ◽  
Hee Jong Jeong ◽  
Jeong Sik Rim ◽  
Min Cheol Joo

1990 ◽  
Vol 30 ◽  
pp. S71-S77 ◽  
Author(s):  
W.C. de Groat ◽  
M. Kawatani ◽  
T. Hisamitsu ◽  
C.-L. Cheng ◽  
C.-P. Ma ◽  
...  

2014 ◽  
Vol 38 (4) ◽  
pp. 433 ◽  
Author(s):  
Kang Keun Lee ◽  
Moon Young Lee ◽  
Dong Yeop Han ◽  
Hee Jong Jung ◽  
Min Cheol Joo

Sign in / Sign up

Export Citation Format

Share Document