Urethral closure mechanisms under sneeze-induced stress condition in rats: a new animal model for evaluation of stress urinary incontinence

2003 ◽  
Vol 285 (2) ◽  
pp. R356-R365 ◽  
Author(s):  
Izumi Kamo ◽  
Kazumasa Torimoto ◽  
Michael B. Chancellor ◽  
William C. de Groat ◽  
Naoki Yoshimura
Keyword(s):  
Urinary Incontinence ◽  
Stress Condition ◽  
Female Rats ◽  
Urinary Continence ◽  
Abdominal Pressure ◽  
Intravesical Pressure ◽  
External Urethral Sphincter ◽  
Urinary Leakage ◽  
Induced Stress ◽  
Urethral Closure

The urethral closure mechanism under a stress condition induced by sneezing was investigated in urethane-anesthetized female rats. During sneezing, while the responses measured by microtip transducer catheters in the proximal and middle parts of the urethra increased, the response in the proximal urethra was almost negligible when the bladder response was subtracted from the urethral response or when the abdomen was opened. In contrast, the response in the middle urethra during sneezing was still observed after subtracting the bladder response or after opening the abdomen. These responses in the middle urethra during sneezing were significantly reduced ∼80% by bilateral transection of the pudendal nerves and the nerves to the iliococcygeous and pubococcygeous muscles but not by transection of the visceral branches of the pelvic nerves and hypogastric nerves. The sneeze leak point pressure was also measured to investigate the role of active urethral closure mechanisms in maintaining total urethral resistance against sneeze-induced urinary incontinence. In sham-operated rats, no urinary leakage was observed during sneeze, which produced an increase of intravesical pressure up to 37 ± 2.2 cmH2O. However, in nerve-transected rats urinary leakage was observed when the intravesical pressure during sneezing exceeded 16.3 ± 2.1 cmH2O. These results indicate that during sneezing, pressure increases elicited by reflex contractions of external urethral sphincter and pelvic floor muscles occur in the middle portion of the urethra. These reflexes in addition to passive transmission of increased abdominal pressure significantly contribute to urinary continence mechanisms under a sneeze-induced stress condition.

Urethral closure mechanisms during sneezing-induced stress in anesthetized female cats

2007 ◽  
Vol 293 (3) ◽  
pp. R1357-R1367 ◽  
Author(s):  
V. Julia-Guilloteau ◽  
P. Denys ◽  
J. Bernabé ◽  
K. Mevel ◽  
E. Chartier-Kastler ◽  
...  
Keyword(s):  
Open Abdomen ◽  
Levator Ani ◽  
Urinary Continence ◽  
Abdominal Pressure ◽  
External Urethral Sphincter ◽  
Relevant Model ◽  
Induced Stress ◽  
Pharmacological Studies ◽  
Urethral Closure ◽  
Lower Urinary

During stress-induced increase in abdominal pressure, urinary continence is maintained by urethral closure mechanisms. Active urethral response has been studied in dogs and rats. Such an active urethral response is also believed to occur in humans during stress events. We aimed to investigate urethral closure mechanisms during sneezing in cats. Urethral pressures along the urethra (UP1–UP4), with microtip transducer catheters with UP4 positioned in the distal urethra where the external urethral sphincter (EUS) is located, and intravesical pressure were measured, and abdominal wall, anal sphincter (AS), levator ani (LA), and EUS electromyograms (EMGs) were recorded during sneezing under closed-abdomen and open-abdomen conditions in eight anesthetized adult female cats. Proximal and middle urethral response induced by sneezing was not different from bladder response. Distal urethral response was greater compared with proximal and middle urethral and bladder response. In the open-abdomen bladder, proximal and middle urethral responses were similarly decreased and distal urethral response was unchanged compared with the closed-abdomen bladder. Bladder and urethral responses were positively correlated to sneeze strength. EUS, LA, and AS EMGs increased during sneezing. No urine leakage was observed, regardless of the strength of sneeze. In cats urethral closure mechanisms are partly passive in the proximal and middle urethra and involve an active component in the distal urethra that is believed to result from EUS and possibly LA contractions. Because central serotonin exerts similar effects on the lower urinary tract in cats and humans, the cat may represent a relevant model for pharmacological studies on continence mechanisms.

Role of vasopressin V1A receptor in the urethral closure reflex in rats

2011 ◽  
Vol 300 (4) ◽  
pp. F976-F982 ◽  
Author(s):  
Hiroyuki Ueno ◽  
Masako Kuno ◽  
Yasushi Shintani ◽  
Izumi Kamo
Keyword(s):  
Spinal Cord ◽  
Pressure Rise ◽  
Physiological Role ◽  
Female Rats ◽  
Reflex Response ◽  
Abdominal Pressure ◽  
Intravesical Pressure ◽  
Urethral Closure ◽  
Urethral Resistance ◽  
Vasopressin V1a Receptor

An enhanced urethral closure reflex via the spinal cord is related to urethral resistance elevation during increased abdominal pressure. However, with the exception of monoamines, neurotransmitters modulating this reflex are not understood. We investigated whether the vasopressin V1A receptor (V1AR) is involved in the urethral closure reflex in urethane-anesthetized female rats. V1AR mRNA was highly expressed among the vasopressin receptor family in the total RNA purified from lamina IX in the spinal cord L6–S1 segment. In situ hybridization analysis of the spinal L6–S1 segment confirmed that these positive signals from the V1ARs were only detected in lamina IX. Intrathecally injected Arg8-vasopressin (AVP), an endogenous ligand, significantly increased urethral resistance during an intravesical pressure rise, and its effect was blocked by the V1AR antagonist. AVP did not increase urethral resistance in rats in which the pelvic nerves were transected bilaterally. Urethral closure reflex responses to the intravesical pressure rise increased by up to threefold compared with the baseline response after AVP administration in contrast to no increase by vehicle. In addition, intravenously and intrathecally injected V1AR antagonists decreased urethral resistance. These results suggest that V1AR stimulation in the spinal cord enhances the urethral closure reflex response, thereby increasing urethral resistance during an abdominal pressure rise and that V1AR plays a physiological role in preventing urine leakage.

Involvement of reflex urethral closure mechanisms in urethral resistance under momentary stress condition induced by electrical stimulation of rat abdomen

2007 ◽  
Vol 293 (3) ◽  
pp. F920-F926 ◽  
Author(s):  
Izumi Kamo ◽  
Tadatoshi Hashimoto
Keyword(s):  
Urinary Incontinence ◽  
Electrical Stimulation ◽  
Abdominal Pressure ◽  
Intravesical Pressure ◽  
Leak Point Pressure ◽  
Pelvic Nerves ◽  
Urethral Closure ◽  
Urethral Resistance ◽  
Point Pressure ◽  
Stimulation Of

A novel method for evaluating the urethral resistance during abrupt elevation of abdominal pressure was developed in spinalized female rats under urethane anesthesia. Electrical stimulation of abdominal muscles for 1 s induced increases in both the intra-abdominal and the intravesical pressure in a stimulus-dependent manner, and the bladder response was almost lost when the abdomen was opened. The lowest intravesical pressure during electrical stimulation that induced fluid leakage from the urethral orifice (leak point pressure) and the maximal intravesical pressure without urine leakage below the leak point pressure were evaluated as the indexes of urethral resistance. Lower urethral resistance was obtained in the rats whose pelvic nerves or somatic nerves containing pudendal nerves and nerves to iliococcygeus/pubococcygeus muscles were transected bilaterally. In contrast, transection of bilateral hypogastric nerves showed smaller effects. Duloxetine, a drug for stress urinary incontinence, enlarged the reflex urethral closing contractions that were induced by an increase in intravesical pressure and measured using a microtip transducer catheter in the middle urethra. This drug also increased the urethral resistance (leak point pressure), whereas it did not show any effect in the rats whose pelvic nerves were bilaterally transected, showing that the augmentation of the reflex urethral closure by the drug resulted in the elevation of the urethral resistance. From these findings, it was concluded that during momentary elevation of abdominal pressure, the reflex urethral closure mechanisms via bladder-spinal cord-urethral sphincter and pelvic floor muscles greatly contribute to the increase in the urethral resistance to prevent the urinary incontinence.

scholarly journals Stress Incontinence during Different High-Impact Exercises in Women: A Pilot Survey

2020 ◽  
Vol 17 (22) ◽  
pp. 8372
Author(s):  
Iman Akef Khowailed ◽  
Joelle Pinjuv-Turney ◽  
Cathy Lu ◽  
Haneul Lee
Keyword(s):  
Urinary Incontinence ◽  
Stress Urinary Incontinence ◽  
Boot Camp ◽  
High Impact ◽  
Abdominal Pressure ◽  
Online Questionnaire ◽  
Pilot Survey ◽  
Urinary Leakage ◽  
Nulliparous Women ◽  
Significant Difference

The aim of this survey was to investigate the prevalence of stress urinary incontinence (SUI) among women (primigravida, multigravida, and nulligravida) in high-impact exercise groups—CrossFit, kickboxing, and boot camp. Incontinence Survey was modified to an anonymous online questionnaire. A total of 17 participants, 64.2% reported at least some urinary leakage during exercise. About 85.7% of participants in each of the 3 high-intensity exercise groups exercised >3 h/week. There was no significant difference in the likelihood of urinary leakage between participants who have had at least 1 pregnancy and those who had never been pregnant. CrossFit group were significantly more likely to report urinary leakage than those in the kickboxing and boot camp groups combined (p = 0.023). The participants did not exhibit typical risk factors, as they were premenopausal, active, and had an average body mass index within the normal range. This pilot survey indicates that all women those who do high-impact exercises are susceptible to stress urinary incontinence (SUI), and that CrossFit poses a greater risk for SUI in terms of more jumping resulting in increased intra-abdominal pressure and ground reaction forces compared to others. Our pilot study indicates that a higher risk of SUI during high impact exercises may exist associated with previous pregnancy but also in nulliparous women.

scholarly journals Urethral closure occurs by recoiling, pressure transmission, and a guarding reflex

2020 ◽  
Vol 31 (11) ◽  
pp. 2447-2449
Author(s):  
Bo S. Bergström
Keyword(s):  
Urinary Incontinence ◽  
Stress Urinary Incontinence ◽  
Integral Theory ◽  
Female Stress Urinary Incontinence ◽  
Abdominal Pressure ◽  
Pressure Transmission ◽  
Urethral Closure

AbstractEnhörning’s abdominal pressure transmission theory (ET) is built on Pascal’s law of fluid pressures. A theory that rejects ET also rejects this basic physical law and cannot be considered scientifically sound. The integral theory (IT) of female stress urinary incontinence rejects ET. This issue is discussed from the viewpoint of the urethral hanging theory of female stress urinary incontinence (UHT).

scholarly journals Time course for urethral neuromuscular reestablishment and its facilitated recovery by transcutaneous neuromodulation after simulated birth trauma in rats

2021 ◽  
Author(s):  
José L. Palacios ◽  
Ricardo Juárez ◽  
Nancy Mirto-Aguilar ◽  
Alvaro Munoz ◽  
Margot S. Damaser ◽  
...  
Keyword(s):  
Urinary Incontinence ◽  
Time Course ◽  
Birth Trauma ◽  
Urinary Continence ◽  
Transcutaneous Electrical Stimulation ◽  
Urethral Sphincter ◽  
External Urethral Sphincter ◽  
Dorsal Nerve ◽  
Urine Leakage ◽  
Vaginal Distension

Abstract The aims of the study were to determine the time-course of urinary incontinence recovery after vaginal distension (VD), elucidate the mechanisms of injury from VD leading to external urethral sphincter (EUS) dysfunction, and assess if transcutaneous electrical stimulation (TENS) of the dorsal nerve of the clitoris facilitates recovery of urinary continence after VD. Rats underwent 4-h VD, 4-h sham VD (SH-VD), VD plus 1-h DNC TENS, and VD plus 1-h sham TENS (SH-TENS). TENS or SH-TENS were applied immediately and at days 2 and 4 post-VD. Micturition behavior, urethral histochemistry and histology, EUS and nerve electrophysiology, and cystometrograms were evaluated. VD induced urine leakage and disrupted EUS fibers and nerve-conduction. Urine leakage disappeared 13 days post-VD. Structural and functional recovery of the EUS neuromuscular circuitry started by day 6 post-VD but did not fully recovered by day 11 post-VD. TENS significantly decreased the frequency of urine leakage post-VD (p<0.01). We conclude that rat urinary continence function after VD requires 2 weeks to recover, although urethra structure is not fully recovered. Treatment to facilitate neuroregeneration should be applied within one-week after damage. TENS facilitated urinary continence recovery after VD. This treatment may have potential to decrease postpartum urinary incontinence in women.

Pathway to Finite Element Analysis of Stress Urinary Incontinence Mechanics

2011 ◽  
Author(s):  
Thomas Spirka ◽  
Kimberly Kenton ◽  
Linda Brubaker ◽  
Margot Damaser
Keyword(s):  
Finite Element Analysis ◽  
Finite Element ◽  
Urinary Incontinence ◽  
Stress Urinary Incontinence ◽  
Bladder Pressure ◽  
Abdominal Pressure ◽  
Element Analysis ◽  
Urethral Closure Pressure ◽  
Bladder Contraction ◽  
Urethral Closure

Stress urinary incontinence (SUI), a condition that affects mainly women, is characterized by the involuntary leakage of urine caused by an increase in abdominal pressure in the absence of a bladder contraction that raises the vesical (bladder) pressure to a level that exceeds the urethral closure pressure.

scholarly journals Somatomotor and sensory urethral control of micturition in female rats

2014 ◽  
Vol 307 (11) ◽  
pp. F1207-F1214 ◽  
Author(s):  
Yolanda Cruz ◽  
César Pastelín ◽  
Brian M. Balog ◽  
Paul J. Zaszczurynski ◽  
Margot S. Damaser
Keyword(s):  
Peak Pressure ◽  
Sensory Innervation ◽  
Female Rats ◽  
Urinary Continence ◽  
Emg Activity ◽  
Detailed Knowledge ◽  
External Urethral Sphincter ◽  
Motor Branch ◽  
Contraction Duration ◽  
Dorsal Nerve

In rats, axons of external urethral sphincter (EUS) motoneurons travel through the anastomotic branch of the pudendal nerve (ABPD) and anastomotic branch of the lumbosacral trunk (ABLT) and converge in the motor branch of the sacral plexus (MBSP). The aim of the present study was to determine in female rats the contribution of these somatomotor pathways and urethral sensory innervation from the dorsal nerve of the clitoris on urinary continence and voiding. EUS electromyographic (EMG) activity during cystometry, leak point pressure (LPP), and voiding efficiency (VE) were assessed in anesthetized virgin Sprague-Dawley female rats before and after transection of the above nerve branches. Transection of the MBSP eliminated EUS EMG, decreased LPP by 50%, and significantly reduced bladder contraction duration, peak pressure, intercontraction interval, and VE. Transection of the ABPD or ABLT decreased EUS EMG discharge and LPP by 25% but did not affect VE. Transection of the dorsal nerve of the clitoris did not affect LPP but reduced contraction duration, peak pressure, intercontraction interval, and VE. We conclude that somatomotor control of micturition is provided by the MBSP with axons travelling through the ABPD and ABLT. Partial somatomotor urethral denervation induces mild urinary incontinence, whereas partial afferent denervation induces voiding dysfunction. ABPD and ABLT pathways could represent a safeguard ensuring innervation to the EUS in case of upper nerve damage. Detailed knowledge of neuroanatomy and functional innervation of the urethra will enable more accurate animal models of neural development, disease, and dysfunction in the future.

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