Effect of vaginal distension on blood flow and hypoxia of urogenital organs of the female rat

Damaser, Margot S.; Whitbeck, Catherine; Chichester, Paul; Levin, Robert M.

doi:10.1152/japplphysiol.01071.2004

Cited by 71 publications

(70 citation statements)

References 41 publications

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“…The biomechanical changes observed in our model for acute SUI may stem from functional, structural, neural, or vascular alterations that result from VD (1,5,9,13). Previous in vivo investigations using a similar model showed that simulated birth trauma produces lower bladder leak-point pressures compared with healthy controls (5).…”

Section: Discussionmentioning

confidence: 85%

“…The observed biomechanical changes may also stem from damaged lower urinary tract vasculature. Using a rat model similar to the one used in the current work, Damaser et al (9) studied blood flow to three major pelvic organs: bladder, vagina, and the urethra. The bladder and the urethra experienced periods of hypoxia during VD, which can greatly affect the urothelium and neuromuscular components of this tissue.…”

Section: Discussionmentioning

confidence: 99%

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Ex vivo biomechanical properties of the female urethra in a rat model of birth trauma

Prantil

Jankowski

Kaiho³

et al. 2007

American Journal of Physiology-Renal Physiology

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Prantil RL, Jankowski RJ, Kaiho Y, de Groat WC, Chancellor MB, Yoshimura N, Vorp DA. Ex vivo biomechanical properties of the female urethra in a rat model of birth trauma. Am J Physiol Renal Physiol 292: F1229 -F1237, 2007. First published December 26, 2006; doi:10.1152/ajprenal.00292.2006.-Stress urinary incontinence (SUI) is the involuntary release of urine during sudden increases in abdominal pressures. SUI is common in women after vaginal delivery or pelvic trauma and may alter the biomechanical properties of the urethra. Thus we hypothesize that injury due to vaginal distension (VD) decreases urethral basal tone and passive stiffness. This study aimed to assess the biomechanical properties of the urethra after VD in the baseline state, where basal muscle tone and extracellular matrix (ECM) are present, and in the passive state, where inactive muscle and ECM are present. Female rat urethras were isolated in a rat model of acute SUI induced by simulated birth trauma. Our established ex vivo system was utilized, wherein we applied intraluminal static pressures ranging from 0 to 20 mmHg. Outer diameter was measured via a laser micrometer. Measurements were recorded via computer. Urethral thickness was assessed histologically. Stress-strain responses of the urethra were altered by VD. Quantification of biomechanical parameters indicated that VD decreased baseline stiffness. The passive peak incremental elastic modulus of the distal segment in VD urethras was less than for controls (1.84 Ϯ 0.67 vs. 1.19 Ϯ 0.70 ϫ 10 6 dyne/cm 2 , respectively; P ϭ 0.016). An increase was noted in passive lowpressure compliance values in proximal VD urethras compared with controls (9.44 Ϯ 2.43 vs. 4.62 Ϯ 0.60 mmHg Ϫ1 , respectively; P ϭ 0.04). Biomechanical analyses suggest that VD alters urethral basal tone, proximal urethral compliance, and distal stiffness. Lack of basal smooth muscle tone, in combination with these changes in the proximal and distal urethra, may contribute to SUI induced by VD. stress urinary incontinence; sphincter; collagen COSTS FOR URINARY INCONTINENCE exceed $16 billion annually, and stress urinary incontinence (SUI) is the most common type of urinary incontinence among middle-aged women (25,26). SUI is associated with weakened and overstretched muscles and connective tissues, which lead to reduced muscle tension in the urethral sphincter complex. This results in the inability of the urethra to close tightly during increased abdominal pressure. Particularly in younger women, neuromuscular injury during vaginal birth often causes disorders involving sphincteric mechanisms (30). The incidence of intrinsic sphincter deficiency was recently found to be greater than previously thought (18), and previous clinical studies suggested that impaired urethral closure mechanisms contribute to intrinsic sphincter deficiency in SUI.Decreased electromyographic activity of the striated urethral sphincter muscle has been detected in middle-aged women with SUI (37). Using a rat model of birth trauma, Resplande et al. (28) ...

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Ex vivo biomechanical properties of the female urethra in a rat model of birth trauma

Prantil

Jankowski

Kaiho³

et al. 2007

American Journal of Physiology-Renal Physiology

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“…In that position, the balloon compressed the organs of the pelvic area (pelvic vagina, pelvic urethra, rectum, pelvic floor muscles, and its vessels and nerves) against the pelvic bone and distended the perineal genitourinary tract (distal region of the vagina and urethra and the vessels and nerves related to them). Thus, the VD model in rats produces direct mechanical damage to the pelvic urethra and distal genitourinary tract, which may explain the resultant disorganization and thinness of the EUS (4, 39) and the physiological impairment observed after VD, such as hypoxia of the genitourinary organs, indicating a reduction in blood flow (9), abolished EUS activity (21), decreased leak point pressure, and/or urine leakage with effort, suggesting urethral closure incompetence (26, …”

Section: Discussionmentioning

confidence: 99%

“…A prolonged parturition can be modeled with VD of greater duration than the duration of parturition in intact rats (19,34). Using the VD model, investigators have demonstrated bladder, urethral, and vaginal hypoxia (9), anatomic and functional damage to the EUS and its innervation (4,21), and decreases in urethral resistance (26). Whether these VDinduced structural and functional changes are sufficient to cause signs of voiding dysfunction in awake animals is unknown.…”

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confidence: 99%

Neuroanatomic and behavioral correlates of urinary dysfunction induced by vaginal distension in rats

Palacios-Galicia

Juárez

Morán

et al. 2016

American Journal of Physiology-Renal Physiology

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-The aim of the present study was to use a model of simulated human childbirth in rats to determine the damage to genitourinary structures and behavioral signs of urinary dysfunction induced by vaginal distension (VD) in female rats. In experiment 1, the length of the genitourinary tract and the nerves associated with it were measured immediately after simulated human delivery induced by VD or sham (SH) procedures. Electroneurograms of the dorsal nerve of the clitoris (DNC) were also recorded. In experiment 2, histological characteristics of the bladder and major pelvic ganglion of VD and SH rats were evaluated. In experiment 3, urinary parameters were determined in conscious animals during 6 h of dark and 6 h of light before and 3 days after VD or SH procedures. VD significantly increased distal vagina width (P Ͻ 0.001) and the length of the motor branch of the sacral plexus (P Ͻ 0.05), DNC (P Ͻ 0.05), and vesical nerves (P Ͻ 0.01) and decreased DNC frequency and amplitude of firing. VD occluded the pelvic urethra, inducing urinary retention, hematomas in the bladder, and thinness of the epithelial (P Ͻ 0.05) and detrusor (P Ͻ 0.01) layers of the bladder. Major pelvic ganglion parameters were not modified after VD. Rats dripped urine in unusual places to void, without the stereotyped behavior of micturition after VD. The neuroanatomic injuries after VD occur alongside behavioral signs of urinary incontinence as determined by a new behavioral tool for assessing micturition in conscious animals. external urethral sphincter; dorsal nerve of the clitoris; major pelvic ganglion; micturition MICTURITION consists of two phases: storage and urine expulsion. During storage, the detrusor is relaxed while the bladder neck and urethra are activated, preventing involuntary bladder emptying (11). Extrinsic elements such as the levator ani muscle also contribute to the maintenance of continence (3). When the bladder reaches its threshold volume, spinal and supraspinal reflexes are triggered to induce bladder contraction and urethral relaxation, and urine flows through the urethra (11). Damage to the lower urinary tract and/or its innervation can induce urinary dysfunction (3,29,41).Urinary dysfunction affects the health of many women (60). Stress urinary incontinence has been described as involuntary loss of urine during effort and is the most prevalent urinary disorder related to vaginal childbirth, which is known to injure the pudendal nerve and denervate the external urethral sphincter (EUS) (3, 15, 57).Maternal pelvic viscera and nerve damage results from the difficulty of human childbirth due the large fetal head and brain relative to the maternal pelvis size. Neonates at birth have heads that are close to the size of the maternal birth canal through which they must pass during the second stage of parturition (48). Births of fetuses over 4 kg or fetal malposition often prolong parturition (30), retaining the fetus in the pelvic cavity, the main anatomic resistance to fetal expulsion. Prolonged second stage of parturition...

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“…This finding was echoed by Cannon et al (6), who showed that increased duration of vaginal distention and multiple vaginal deliveries also decreased leak point pressures and increased anatomical injury. It may be that the distention causes ischemia to the urethra or that there is reperfusion injury after the vaginal distention has resolved (8). A similar mechanism of injury may be operative in the connective tissues of the vaginal wall.…”

Section: Discussionmentioning

confidence: 99%

Effect of vaginal distention on elastic fiber synthesis and matrix degradation in the vaginal wall: potential role in the pathogenesis of pelvic organ prolapse

Rahn¹,

Acevedo²,

Word³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Rahn DD, Acevedo JF, Word RA. Effect of vaginal distention on elastic fiber synthesis and matrix degradation in the vaginal wall: potential role in the pathogenesis of pelvic organ prolapse. Am J Physiol Regul Integr Comp Physiol 295: R1351-R1358, 2008. First published July 16, 2008 doi:10.1152/ajpregu.90447.2008 activity is increased in the postpartum vagina of wild-type (WT) animals. This degradative activity is also accompanied by a burst in elastic fiber synthesis and assembly. The mechanisms that precipitate these changes are unclear. The goals of this study were to determine how vaginal distention (such as in parturition) affects elastic fiber homeostasis in the vaginal wall and the potential significance of these changes in the pathogenesis of pelvic organ prolapse. Vaginal distention with a balloon simulating parturition resulted in increased MMP-2 and MMP-9 activity in the vaginal wall of nonpregnant and pregnant animals. This was accompanied by visible fragmented and disrupted elastic fibers in the vaginal wall. In nonpregnant animals, the abundant amounts of tropoelastin and fibulin-5 in the vagina were not increased further by distention. In contrast, in pregnant animals, the suppressed levels of both proteins were increased 3-fold after vaginal distention. Distention performed in fibulin-5-deficient (Fbln5 Ϫ/Ϫ ) mice with defective elastic fiber synthesis and assembly induced accelerated pelvic organ prolapse, which never recovered. We conclude that, in pregnant mice, vaginal distention results in increased protease activity in the vaginal wall but also increased synthesis of proteins important for elastic fiber assembly. Distention may thereby contribute to the burst of elastic fiber synthesis in the postpartum vagina. The finding that distention results in accelerated pelvic organ prolapse in Fbln5 Ϫ/Ϫ animals, but not in WT, indicates that elastic fiber synthesis is crucial for recovery of the vaginal wall from distention-induced increases in vaginal protease activity. childbirth trauma; MMP9; protease; pregnancy PELVIC ORGAN PROLAPSE IS A common problem for women with significant psychological, social, and financial implications (12,26,29). Whereas many factors appear to incite or promote the progression of prolapse, the two major risk factors for pelvic organ prolapse are history of vaginal delivery and aging. Although cesarean delivery does not completely protect the pelvic floor from the adverse effects of pregnancy, it is universally agreed that vaginal delivery has a deleterious impact on the development of pelvic organ prolapse in women, and this impact may not be of clinical significance until decades after delivery. The mechanisms by which childbirth leads to failure of pelvic organ support, however, are not well understood (3,26).Mice with null mutations in genes encoding lysyl oxidase like 1 (LOXL1) (15, 16) or fibulin-5 (FBLN5) (11) develop pelvic organ prolapse. Since both proteins play important roles in elastic fiber synthesis and assembly (19,30), these findings indicate that fa...

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Effect of vaginal distension on blood flow and hypoxia of urogenital organs of the female rat

Cited by 71 publications

References 41 publications

Ex vivo biomechanical properties of the female urethra in a rat model of birth trauma

Ex vivo biomechanical properties of the female urethra in a rat model of birth trauma

Neuroanatomic and behavioral correlates of urinary dysfunction induced by vaginal distension in rats

Effect of vaginal distention on elastic fiber synthesis and matrix degradation in the vaginal wall: potential role in the pathogenesis of pelvic organ prolapse

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