Pubo-Urethral Ligament Transection Causes Stress Urinary Incontinence in the Female Rat: A Novel Animal Model of Stress Urinary Incontinence

Kefer, John C.; Liu, Guiming; Daneshgari, Firouz

doi:10.1016/j.juro.2007.09.025

Cited by 24 publications

(27 citation statements)

References 18 publications

(31 reference statements)

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“…29 SUI occurs predominantly in women, and consequently female animals are promoted for model development. Various interventions have been used to damage urethral nerve and muscle to impair urethral resistance, namely; vaginal distension 30 to mimic trauma of child birth; pudendal or hypogastric neurectomy 31,32 to mimic neuropathy; and increasing urethral mobility by freeing the bladder and urethra from surrounding connective tissue 33 to mimic pelvic organ prolapse, which is often associated with SUI. Indeed, these animal models produce a decrease in urethral resistance when tested in terminally anaesthetized animals, even weeks after the insult.…”

Section: Stress Urinary Incontinence (Sui)mentioning

confidence: 99%

Animal models and their use in understanding lower urinary tract dysfunction

Fry

Daneshgari

Thor³

et al. 2010

Neurourology and Urodynamics

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This review will highlight appropriate animal models for the study of a number of disorders involving changes to lower urinary tract function. A major hurdle to the development of animal models for human lower urinary tract disorders is that the clinical pathophysiology of the latter mostly remain idiopathic. Acute injury/inflammation of otherwise healthy animals has often been used to study effects on a target tissue/organ. However, these "acute" models may not adequately address the characteristics of "chronic" visceral disorders. In addition, the relevance of observed changes following acute injury/inflammation, in terms of possible therapeutic targets, may not reflect that which occurs in the human condition. We have therefore emphasized the situations when animal models are required to investigate lower urinary tract disorders and what they should set out to achieve. In particular we have discussed the merits and disadvantages of a number of paradigms that set out to investigate specific lower urinary tract disorders or situations associated with these conditions. These include animal models of overactive bladder, stress urinary incontinence, ageing and congenital defects of the urinary tract and bladder pain syndrome.

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Section: Stress Urinary Incontinence (Sui)mentioning

confidence: 99%

Animal models and their use in understanding lower urinary tract dysfunction

Fry

Daneshgari

Thor³

et al. 2010

Neurourology and Urodynamics

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“…This is supported by clinical data demonstrating that direct urethral injury occurs at higher rates in women delivering vaginally rather than by cesarean section [39]. Injury models such as urethrolysis, pubourethral ligament transection and electrocauterization of the EUS have been employed in rats to reproduce such trauma [31,40,41]. In the urethrolysis model, the length of the urethra is freed from the surrounding tissues, including the endopelvic fascia and anterior vaginal wall, beginning at its proximal end [31].…”

Section: Animal Models Of Postpartum Sui and Simulated Childbirth Injurymentioning

confidence: 95%

“…In the urethrolysis model, the length of the urethra is freed from the surrounding tissues, including the endopelvic fascia and anterior vaginal wall, beginning at its proximal end [31]. Similarly, transection of the pubourethral ligament results in a similar detachment and hypermobility of the urethra [40]. In the electrocauterization model, tissue lateral to the midurethra is cauterized, producing both muscle and nerve damage at that location [41].…”

Section: Animal Models Of Postpartum Sui and Simulated Childbirth Injurymentioning

confidence: 99%

“…Methods utilizing this technique vary from a closed abdominal approach to an open abdominal approach with direct bladder visualization [26,28,46]. Bladder pressure during compression can be recorded using either suprapubic or urethral catheters, with the latter contributing to urethral resistance [40,42]. While a straightforward method, factors such as angle of compression, speed of compression and bladder size may impact measurements.…”

Section: Animal Models Of Postpartum Sui and Simulated Childbirth Injurymentioning

confidence: 99%

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Postpartum stress urinary incontinence: lessons from animal models

Gill

Moore

Damaser³

2010

Expert Review of Obstetrics & Gynecology

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Postpartum stress urinary incontinence (SUI) is associated with chronic SUI in later life, which is 240% more likely to occur in women who deliver vaginally than those who did not. The etiology of SUI is multifactoral and has been associated with defects in both neuromuscular and structural components of continence. Specifically, clinical studies have demonstrated that pudendal nerve damage occurs during vaginal delivery, supporting the concept that neuromuscular damage to the continence mechanism can result in postpartum SUI. Urethral hypermobility and the loss of pelvic floor support, such as that involved in pelvic organ prolapse, have also been associated with SUI. Animal models provide an opportunity to investigate these injuries, individually and in combination, enabling researchers to gain further insight into their relative contributions to the development of SUI and the effectiveness of potential therapies for it. This article discusses the use of animal models of postpartum SUI in addition to the broad insights into treatment efficacy they provide. Keywords birth injury; continence; muscle injury; nerve injury; neuromuscular; regeneration; repair Clinical relevance of animal modelsEstimates of the prevalence of stress urinary incontinence (SUI) vary with differences in population samples and methods of statistical adjustment. Despite this variability, large epidemiological studies have established that SUI is approximately 240% more prevalent in women who underwent vaginal delivery compared with women who underwent cesarean section [1,2]. There also exists a strong association between antenatal SUI and postpartum SUI for primiparae [3][4][5]. Recent research has demonstrated that women who develop SUI during pregnancy are 579% more likely to have SUI 1 year postpartum [6]. Both antenatal and immediate postpartum SUI are predictive of chronic SUI. A total of 73% of women having SUI 3 months postpartum are incontinent 6 years postpartum [7][8][9][10]. Thus, a clear link exists between vaginal delivery and SUI, both immediately postpartum and later in life.Conceptually, the urinary continence mechanism can be thought of as having two major components. The first is structural, the physical support of the urinary tract, and composed of †

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“…5,8,9 VD mimics the non-specific trauma associated with the second stage of labor in women whereas pudendal nerve crush and PNT aim to simulate the nerve injury observed with vaginal delivery directly. All of these models, either alone or in combination, result in a significant decrease in urethral resistance to leakage, indicative of SUI.…”

Section: Introductionmentioning

confidence: 99%

Stem Cell Homing Factor, CCL7, Expression in Mouse Models of Stress Urinary Incontinence

Hijaz

Grimberg

Tao

et al. 2013

Female Pelvic Medicine &Amp; Reconstructive Surgery

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Objectives Animal models of vaginal distention (VD) have demonstrated increased expression of chemokine (C-C motif) ligand 7 (CCL7). In this study, we investigated the expression of CCL7 in mice models of simulated birth trauma-induced urinary incontinence utilizing VD and pudendal nerve transection (PNT). Methods Forty-nine mice were divided into 6 groups: VD, sham VD, PNT, sham PNT anesthesia, and age-matched controls. The urethra, vagina, and rectum were harvested for the expression of CCL7 immediately or 24 hours after assigned procedure. Venous sampling for quantification of serum CCL7 was also performed. An ANOVA model was used to compare the relative expression of CCL7 in each group. Results Urethral CCL7 expression in the VD group was significantly higher than control group after 24 hours (p<0.01). There was no difference in the urethral CCL7 expression in PNT, sham PNT, sham VD or anesthesia groups compared with controls. No statistically significant difference was noted in the vaginal and rectal expression of CCL7 between any of the groups except for sham PNT. Statistically significant differences were noted in the serum CCL7 expression in VD, PNT and sham PNT (p<0.01 in all) groups after 24 hours compared with the control group. Conclusions This study demonstrates over-expression of urethral CCL7 after VD but not PNT. This suggests that nerve injury does not contribute to the CCL7 over-expression. The over-expression of CCL7 in the serum of mice after VD suggests a translational potential where CCL7 measurement could be used as a surrogate for injury after delivery.

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Pubo-Urethral Ligament Transection Causes Stress Urinary Incontinence in the Female Rat: A Novel Animal Model of Stress Urinary Incontinence

Cited by 24 publications

References 18 publications

Animal models and their use in understanding lower urinary tract dysfunction

Animal models and their use in understanding lower urinary tract dysfunction

Postpartum stress urinary incontinence: lessons from animal models

Stem Cell Homing Factor, CCL7, Expression in Mouse Models of Stress Urinary Incontinence

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