scholarly journals Dual simulated childbirth injury delays anatomic recovery

2009 ◽  
Vol 296 (2) ◽  
pp. F277-F283 ◽  
Author(s):  
Hui Q. Pan ◽  
James M. Kerns ◽  
Dan L. Lin ◽  
David Sypert ◽  
James Steward ◽  
...  
Keyword(s):  
Pudendal Nerve ◽  
Leak Point Pressure ◽  
External Urethral Sphincter ◽  
Bdnf Expression ◽  
Nerve Crush ◽  
Histological Evidence ◽  
Injury Model ◽  
Point Pressure ◽  
Urethral Function ◽  
Vaginal Distension

A dual childbirth injury model, including vaginal distension (VD) and pudendal nerve crush (PNC), may best represent the injuries seen clinically. The objective of this study was to investigate urethral function, anatomy, and neurotrophin expression after several simulated childbirth injuries. Groups of 140 rats underwent PNC, VD, PNC+VD, or neither (C). Four days after injury, all injury groups had significantly decreased leak-point pressure (LPP) compared with C rats. Ten days after injury, LPP in PNC and PNC+VD rats remained significantly lower than C rats. Three weeks after injury, LPP in all injury groups had recovered to C values. Histological evidence of injury was still evident in the external urethral sphincter (EUS) after VD and PNC+VD 10 days after injury. Three weeks after injury, the EUS of PNC+VD rats remained disrupted. One day after VD, brain-derived neurotrophic factor (BDNF) expression in the EUS was reduced, while neurotrophin-4 (NT-4) and nerve growth factor (NGF) expression was unchanged. BDNF, NT-4, and NGF expression was dramatically upregulated in the EUS after PNC. After PNC+VD, NGF expression was upregulated, and BDNF and NT-4 expression was upregulated somewhat but not to the same extent as after PNC. Ten days after injury, PNC+VD had the least number of normal nerve fascicles near the EUS, followed by PNC and VD. Twenty-one days after injury, all injury groups had fewer normal nerve fascicles, but without significant differences compared with C rats. PNC+VD therefore provides a more severe injury than PNC or VD alone.

scholarly journals Daily bilateral pudendal nerve electrical stimulation improves recovery from stress urinary incontinence

2019 ◽  
Vol 9 (4) ◽  
pp. 20190020 ◽  
Author(s):  
Kangli Deng ◽  
Brian M. Balog ◽  
Dan Li Lin ◽  
Brett Hanzlicek ◽  
Qi-Xiang Song ◽  
...  
Keyword(s):  
Urinary Incontinence ◽  
Electrical Stimulation ◽  
Stress Urinary Incontinence ◽  
Pudendal Nerve ◽  
Sprague Dawley ◽  
External Urethral Sphincter ◽  
Bdnf Expression ◽  
Nerve Crush ◽  
Sprague Dawley Rats ◽  
Point Pressure

Stress urinary incontinence (SUI) in women is strongly associated with childbirth which injures the pudendal nerve (PN) and the external urethral sphincter (EUS) during delivery. Electrical stimulation (ES) can increase brain-derived neurotrophic factor (BDNF) expression in injured neurons, activate Schwann cells and promote neuroregeneration after nerve injury. The aim of this study was to determine if more frequent ES would increase recovery from SUI in a rat model. Forty female Sprague–Dawley rats underwent either sham injury or pudendal nerve crush (PNC) and vaginal distention (VD) to establish SUI. Immediately after injury, electrodes were implanted at the pudendal nerve bilaterally. Each injured animal underwent sham ES, twice per week ES (2/week), or daily ES of 1 h duration for two weeks. Urethral and nerve function were assessed with leak point pressure (LPP), EUS electromyography and pudendal nerve sensory branch potential (PNSBP) recordings two weeks after injury. LPP was significantly increased after daily ES compared to 2/week ES. EUS neuromuscular junction innervation was decreased after injury with sham ES, but improved after 2/week or daily ES. This study demonstrates that daily bilateral ES to the pudendal nerve can accelerate recovery from SUI. Daily ES improved urethral function more than 2/week ES.

scholarly journals Rat Mesenchymal Stem Cell Secretome Promotes Elastogenesis and Facilitates Recovery from Simulated Childbirth Injury

2014 ◽  
Vol 23 (11) ◽  
pp. 1395-1406 ◽  
Author(s):  
Charuspong Dissaranan ◽  
Michelle A. Cruz ◽  
Matthew J. Kiedrowski ◽  
Brian M. Balog ◽  
Bradley C. Gill ◽  
...  
Keyword(s):  
Female Rats ◽  
Urethral Sphincter ◽  
Leak Point Pressure ◽  
External Urethral Sphincter ◽  
Paracrine Factors ◽  
Pelvic Organs ◽  
Point Pressure ◽  
Urethral Smooth Muscle ◽  
And Function ◽  
Vaginal Distension

Vaginal delivery is a risk factor for stress urinary incontinence (SUI). Mesenchymal stem cells (MSCs) home to injured organs and can facilitate repair. The goal of this study was to determine if MSCs home to pelvic organs after simulated childbirth injury and facilitate recovery from SUI via paracrine factors. Three experiments were performed. Eighteen female rats received vaginal distension (VD) or sham VD and labeled intravenous (IV) MSCs to investigate if MSCs home to the pelvic organs. Whole-organ imaging and immunofluorescence were performed 1 week later. Thirty-four female rats received VD and IV MSCs, VD and IV saline, or sham VD and IV saline to investigate if MSCs accelerate recovery of continence. Twenty-nine female rats received VD and periurethral concentrated conditioned media (CCM), VD and periurethral control media, or sham VD and periurethral control media to investigate if factors secreted by MSCs accelerate recovery from VD. Urethral histology and function were assessed 1 week later. Significantly more MSCs were observed in the urethra, vagina, and spleen after VD compared to sham VD. Continence as measured by leak point pressure (LPP) was significantly reduced after VD in rats treated with saline or control media compared to sham VD but not in those given MSCs or CCM. External urethral sphincter (EUS) function as measured by electromyography (EMG) was not improved with MSCs or CCM. Rats treated with MSCs or CCM demonstrated an increase in elastin fibers near the EUS and urethral smooth muscle more similar to that of sham-injured animals than rats treated with saline or control media. MSCs homed to the urethra and vagina and facilitated recovery of continence most likely via secretion of paracrine factors. Both MSCs and CCM have promise as novel noninvasive therapies for SUI.

scholarly journals Pudendal nerve injury reduces urethral outlet resistance in diabetic rats

2010 ◽  
Vol 299 (6) ◽  
pp. F1443-F1450 ◽  
Author(s):  
Hui Q. Pan ◽  
Dan L. Lin ◽  
Christopher Strauch ◽  
Robert S. Butler ◽  
Vincent M. Monnier ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Pudendal Nerve ◽  
Outlet Obstruction ◽  
Diabetic Rats ◽  
Sprague Dawley ◽  
External Urethral Sphincter ◽  
Nerve Crush ◽  
Point Pressure ◽  
Functional Outlet Obstruction ◽  
Pudendal Nerve Injury

Diabetics have voiding and continence dysfunction to which elevated levels of advanced glycation end products (AGE) may contribute. In addition, pudendal nerve injury is correlated with voiding dysfunction and stress incontinence in rats. The aim of this study was to investigate whether pudendal nerve crush (PNC) in diabetic rats alters urinary function. Female virgin Sprague-Dawley rats (144) were divided equally into diabetic, diuretic, and control groups. Half of the animals in each group were subjected to PNC, and the other half to sham PNC. Diabetes was induced 8 wk before PNC or sham PNC by streptozotocin injection (35 mg/kg). Animals underwent conscious cystometry and leak point pressure (LPP) testing 4 or 13 days after PNC or sham PNC. Tissues of half the animals were tested for levels of AGEs. Qualitative histological assessment was performed in the remaining animals. Diabetic rats 4 days after PNC voided significantly greater volume in a shorter time and with significantly less pressure than after sham PNC, suggesting that diabetic rats have a functional outlet obstruction that is relieved by PNC. LPP was significantly reduced 4 days after PNC in diabetic and diuretic animals and returned to normal 13 days after PNC. Diabetic rats with PNC demonstrated increased muscle fiber disruption and atrophy of the external urethral sphincter. AGEs were significantly elevated in diabetic rats. PNC relieves a functional outlet obstruction in diabetic rats. AGEs are elevated in diabetic rats and could play a role in urinary dysfunction and recovery from PNC.

scholarly journals Effect of a 5-HT1A receptor agonist (8-OH-DPAT) on external urethral sphincter activity in a rat model of pudendal nerve injury

2011 ◽  
Vol 301 (1) ◽  
pp. R225-R235 ◽  
Author(s):  
Shih-Ching Chen ◽  
Chen-Li Cheng ◽  
Wen-Jia Fan ◽  
Jia-Jin Jason Chen ◽  
Chien-Hung Lai ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Rat Model ◽  
Receptor Agonist ◽  
Pudendal Nerve ◽  
Perfusion Pressure ◽  
Urethral Sphincter ◽  
Leak Point Pressure ◽  
External Urethral Sphincter ◽  
Point Pressure ◽  
Pudendal Nerve Injury

Although serotonergic agents have been used to treat patients with stress urinary incontinence, the characteristics of the external urethral sphincter (EUS) activity activated by 5-HT receptors have not been extensively studied. This study examined the effects of the 5-HT1A receptor agonist, 8-hydroxy-2-(di- n-propylamino)tetralin (8-OH-DPAT), on the EUS-electromyography and resistance of the urethra in a rat model with bilateral pudendal nerve injury (BPNI). Two measurements were utilized to assess the effects of the drug on bladder and urethral functions: the simultaneous recordings of transvesical pressure under isovolumetric conditions [isovolumetric intravesical pressure (IVP)] and urethral perfusion pressure, and the simultaneous recordings of IVP during continuously isotonic transvesical infusion with an open urethra (isotonic IVP) and EUS-electromyography. This study also evaluated the urethral continence using leak point pressure testing. The urethral perfusion pressure and leak point pressure measurements of BPNI rats reveal that 8-OH-DPAT significantly increased urethral resistance during the bladder storage phase, yet decreased resistance during the voiding phase. The entire EUS burst period was significantly prolonged, within which the average silent period increased and the frequency of burst discharges decreased. 8-OH-DPAT also improved the voiding efficiency, as evidenced by the detection of decreases in the contraction amplitude and residual volume, with increases in contraction duration and voided volume. These findings suggest that 8-OH-DPAT not only improved continence function, but also elevated the voiding function in a BPNI rat model.

scholarly journals Multiple doses of stem cells maintain urethral function in a model of neuromuscular injury resulting in stress urinary incontinence

2019 ◽  
Vol 317 (4) ◽  
pp. F1047-F1057
Author(s):  
Kristine Janssen ◽  
Dan Li Lin ◽  
Brett Hanzlicek ◽  
Kangli Deng ◽  
Brian M. Balog ◽  
...  
Keyword(s):  
Stem Cells ◽  
Urinary Incontinence ◽  
Single Dose ◽  
Stress Urinary Incontinence ◽  
Pudendal Nerve ◽  
Urethral Sphincter ◽  
External Urethral Sphincter ◽  
Nerve Crush ◽  
Multiple Doses ◽  
Urethral Function

Stress urinary incontinence (SUI) is more prevalent among women who deliver vaginally than women who have had a cesarean section, suggesting that tissue repair after vaginal delivery is insufficient. A single dose of mesenchymal stem cells (MSCs) has been shown to partially restore urethral function in a model of SUI. The aim of the present study was to determine if increasing the number of doses of MSCs improves urethral and pudendal nerve function and anatomy. We hypothesized that increasing the number of MSC doses would accelerate recovery from SUI compared with vehicle treatment. Rats underwent pudendal nerve crush and vaginal distension or a sham injury and were treated intravenously with vehicle or one, two, or three doses of 2 × 106 MSCs at 1 h, 7 days, and 14 days after injury. Urethral leak point pressure testing with simultaneous external urethral sphincter electromyography and pudendal nerve electroneurography were performed 21 days after injury, and the urethrovaginal complex and pudendal nerve were harvested for semiquantitative morphometry of the external urethral sphincter, urethral elastin, and pudendal nerve. Two and three doses of MSCs significantly improved peak pressure; however, a single dose of MSCs did not. Single, as well as repeated, MSC doses improved urethral integrity by restoring urethral connective tissue composition and neuromuscular structures. MSC treatment improved elastogenesis, prevented disruption of the external urethral sphincter, and enhanced pudendal nerve morphology. These results suggest that MSC therapy for postpartum incontinence and SUI can be enhanced with multiple doses.

scholarly journals Transurethral versus suprapubic catheterization to test urethral function in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kristine Janssen ◽  
Kangli Deng ◽  
Steve J. A. Majerus ◽  
Dan Li Lin ◽  
Brett Hanzlicek ◽  
...  
Keyword(s):  
Outlet Obstruction ◽  
Bladder Pressure ◽  
Sprague Dawley ◽  
External Urethral Sphincter ◽  
Emg Amplitude ◽  
Suprapubic Catheterization ◽  
Sphincter Electromyography ◽  
Significant Difference ◽  
Point Pressure ◽  
Urethral Function

AbstractTransurethral and suprapubic catheterization have both been used to test urethral function in rats; however, it is unknown whether these methods affect urethral function or if the order of catheterization affects the results. The aim of this cross-over designed experiment was to compare the effects of catheterization methods and order on leak point pressure (LPP) testing. LPP and simultaneous external urethral sphincter electromyography (EUS EMG) were recorded in anesthetized female virgin Sprague-Dawley rats in a cross-over design to test the effects of transurethral and suprapubic catheterization. There was no significant difference in peak bladder pressure during LPP testing whether measured with a transurethral or suprapubic catheter. There was no significant difference in peak bladder pressure between the first and second catheter insertions. However, peak EMG firing rate, as well as peak EMG amplitude and EMG amplitude difference between peak and baseline were significantly higher after the first catheter insertion compared to the second insertion, regardless of the catheter method. Our results suggest that route of catheterization does not alter urethral function, e.g. create a functional partial outlet obstruction. Either catheterization method could be used for LPP and/or EUS EMG testing in rats.

scholarly journals Electrical stimulation of the pudendal nerve promotes neuroregeneration and functional recovery from stress urinary incontinence in a rat model

2018 ◽  
Vol 315 (6) ◽  
pp. F1555-F1564 ◽  
Author(s):  
Hai-Hong Jiang ◽  
Qi-Xiang Song ◽  
Bradley C. Gill ◽  
Brian M. Balog ◽  
Raul Juarez ◽  
...  
Keyword(s):  
Urinary Incontinence ◽  
Electrical Stimulation ◽  
Stress Urinary Incontinence ◽  
Rat Model ◽  
Pudendal Nerve ◽  
External Urethral Sphincter ◽  
Sham Stimulation ◽  
Point Pressure ◽  
Separate Cohort ◽  
Stimulation Of

The pudendal nerve can be injured during vaginal delivery of children, and slowed pudendal nerve regeneration has been correlated with development of stress urinary incontinence (SUI). Simultaneous injury to the pudendal nerve and its target muscle, the external urethral sphincter (EUS), during delivery likely leads to slowed neuroregeneration. The goal of this study was to determine if repeat electrical stimulation of the pudendal nerve improves SUI recovery and promotes neuroregeneration in a dual muscle and nerve injury rat model of SUI. Rats received electrical stimulation or sham stimulation of the pudendal nerve twice weekly for up to 2 wk after injury. A separate cohort of rats received sham injury and sham stimulation. Expression of brain-derived neurotrophic factor (BDNF) and βII-tubulin expression in Onuf’s nucleus were measured 2, 7, and 14 days after injury. Urodynamics, leak point pressure (LPP), and EUS electromyography (EMG) were recorded 14 days after injury. Electrical stimulation significantly increased expression of BDNF at all time points and βII-tubulin 1 and 2 wk after injury. Two weeks after injury, LPP and EUS EMG during voiding and LPP testing were significantly decreased compared with sham-injured animals. Electrical stimulation significantly increased EUS activity during voiding, although LPP did not fully recover. Repeat pudendal nerve stimulation promotes neuromuscular continence mechanism recovery possibly via a neuroregenerative response through BDNF upregulation in the pudendal motoneurons in this model of SUI. Electrical stimulation of the pudendal nerve may therefore improve recovery after childbirth and ameliorate symptoms of SUI by promoting neuroregeneration after injury.

scholarly journals Diabetes slows the recovery from urinary incontinence due to simulated childbirth in female rats

2007 ◽  
Vol 293 (2) ◽  
pp. R950-R955 ◽  
Author(s):  
Ja-Hong Kim ◽  
Xiao Huang ◽  
Guiming Liu ◽  
Courtenay Moore ◽  
James Bena ◽  
...  
Keyword(s):  
Urinary Incontinence ◽  
External Sphincter ◽  
Bladder Capacity ◽  
Diabetic Rats ◽  
Female Rats ◽  
Sprague Dawley ◽  
Leak Point Pressure ◽  
Sprague Dawley Rats ◽  
Point Pressure ◽  
Vaginal Distension

This study was done to test the hypothesis that simulated vaginal birth by vaginal distension (VD) causes more severe urinary incontinence and slower recovery in diabetic rats. After measuring baseline leak point pressure (LPP) in 16 diabetes mellitus (DM) and 16 age- and weight-matched control (Ct) female Sprague-Dawley rats, these animals underwent either VD or sham VD (sham). Four and ten days after the procedures, LPP and conscious cystometry were assessed. Tissues were then harvested and examined by light microscopy. LPP at baseline was equal among all four groups. Four days after VD, LPP in both VD groups dropped to significantly lower levels than in sham rats ( P < 0.001). Moreover, LPP in the DM+VD group was significantly lower than in the Ct+VD group. At 10 days, LPP in the Ct+VD group had recovered to its baseline value, whereas the LPP in the DM+VD group remained significantly reduced. DM rats had larger bladder capacity and longer voiding intervals than Ct rats. Histological findings included more severe damage to the external sphincter striated musculature of the urethra in DM+VD group compared with Ct+VD. In conclusion, these findings suggest that DM causes increased severity and delayed functional recovery from the effects of simulated childbirth.

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