Alterations of the ex vivo biomechanical properties of the female rat urethra in Spinal Cord Injury (SCI) and Stress Urinary Incontinence (SUI)

2006 ◽  
Vol 39 ◽  
pp. S390
Author(s):  
R. Prantil ◽  
M. Chancellor ◽  
N. Yoshimura ◽  
W. de Groat ◽  
D. Vorp
2018 ◽  
Vol 234 (2) ◽  
pp. 244-251 ◽  
Author(s):  
Azim Patar ◽  
Peter Dockery ◽  
Linda Howard ◽  
Siobhan S. McMahon

2020 ◽  
Vol 3 (1) ◽  
pp. 1-4
Author(s):  
Lin JM ◽  
◽  
Hui Chen ◽  
Liu QL ◽  
Huang MP ◽  
...  

Objective: To evaluate the d the safety and efficacy of 200 U vs. 300 U botulinum toxin A (BTX-A) injections for patients with neurogenic detrusor overactivity (NDO) secondary to spinal cord injury (SCI). Methods: We retrieved the data for the patients who receive a single dose into the detrusor of BTX-A (300 U or 200 U). The clinical outcome included maximum detrusor pressure (Pdetmax) during cystometry, voiding volume, urinary incontinence (UI) episodes between CICs per 24 hour, and complete dryness. Related adverse events were recorded. Results: From July 2015 to June 2017, 28 cases received 300 U BTX-A injections (experiment group) while 19 cases received 200U BTX-A injections (control group). There were no significant differences in baseline evaluation items (gender, age, duration of spinal cord injury, level of neurological injury, AIS scores) between the two groups. There were significant improvement in Pdetmax, UI and I-QoL from baseline in the two groups. Patients in experiment group had statistically greater improvement than those in the control group for Pdetmax (-32.09 cm H2O vs. -28.02 cm H2O, P = 0.016), mean urinary incontinence episodes (-6.18/d vs. -5.01/d, P = 0.042), complete dryness (11 vs. 2, P = 0.031), mean voiding volume (160.52 ml vs. 133.66 ml, P <0.001), and I-QoL (28.53 vs. 20.41, P <0.001). Conclusion: Preliminary results indicate that 300 U BTX-A is more effective than 200 U BTX-A for SCI patients with NDO.


2021 ◽  
Vol 16 (3) ◽  
pp. 550 ◽  
Author(s):  
HyunJoon Lee ◽  
RustemRobertovich Islamov ◽  
FilipOlegovich Fadeev ◽  
FaridVagizovich Bashirov ◽  
VaheArshaluysovich Markosyan ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ken Lee ◽  
Sang O Park ◽  
Pil-Cho Choi ◽  
Seung-Bum Ryoo ◽  
Haeyeong Lee ◽  
...  

AbstractVolume accommodation occurs via a novel mechanism involving interstitial cells in detrusor muscles. The interstitial cells in the bladder are PDGFRα+, and they restrain the excitability of smooth muscle at low levels and prevents the development of transient contractions (TCs). A common clinical manifestation of spinal cord injury (SCI)-induced bladder dysfunction is detrusor overactivity (DO). Although a myogenic origin of DO after SCI has been suggested, a mechanism for development of SCI-induced DO has not been determined. In this study we hypothesized that SCI-induced DO is related to loss of function in the regulatory mechanism provided by PDGFRα+ cells. Our results showed that transcriptional expression of Pdgfra and Kcnn3 was decreased after SCI. Proteins encoded by these genes also decreased after SCI, and a reduction in PDGFRα+ cell density was also documented. Loss of PDGFRα+ cells was due to apoptosis. TCs in ex vivo bladders during filling increased dramatically after SCI, and this was related to the loss of regulation provided by SK channels, as we observed decreased sensitivity to apamin. These findings show that damage to the mechanism restraining muscle contraction during bladder filling that is provided by PDGFRα+ cells is causative in the development of DO after SCI.


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