-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...
Aims To analyze, in female rats, the anatomical and histological features of the urethra and its relationship with the vagina and clitoris, and its innervation. Methods Seventeen adult female Wistar rats were used. Gross anatomy and acetylcholinesterase (AchE) histochemistry were performed to describe the urethral features, adjacent structures, and innervation. The histomorphometric characteristics of the urethra were determined in transversal, longitudinal, or coronal sections stained with Masson's Trichrome. Results The female rat urethra is not a homogeneous tubular organ. The pre‐pelvic and pelvic regions are firmly attached to the vagina with belt‐like striated fibers forming a urethra‐vaginal complex. The bulbar regions have curved segments and a narrow lumen. The clitoral region is characterized by a urethra‐clitoral complex surrounded by a vascular plexus. The lumen area and thickness of the urethral layers significantly varied between regions (P < 0.05). Innervation of the urethra arrives from the major pelvic ganglion, the dorsal nerve of the clitoris (DNC), and the motor branch of the sacral plexus (MBSP). Conclusions Differential tissular composition of the urethra may underlie urinary continence and voiding dysfunction through different physiological mechanisms. The urethra‐vagina complex seems to be the main site controlling urinary continence through active muscular mechanisms, while the bulbar urethra provides passive mechanisms and the urethra‐clitoris complex seems to be crucial for distal urethral closure by means of a periurethral vascular network.
Antecedentes y Objetivos: El Síndrome de Vejiga Hiperactiva (svh) presenta alteraciones motoras como hipertonía de la musculatura del piso pélvico (mpp). El objeto del estudio es demostrar las características de la electromiografía de superficie (emgs) del mpp en el svh tratados con electro-estimulación percutánea del nervio tibial (ptns). Material y Método: Estudio prospectivo, observacional, controlado. Se realizó emgs de mpp a 17 voluntarios con svh rebelde a tratamiento, antes, durante la ptns y 72 horas después. Se asignaron 2 grupos: Catorce voluntarios del grupo ptns, y 3 voluntarios del grupo placebo. Se incluyeron pacientes con evolución mínima de 6 meses, frecuencia urinaria de 8 o más, sin toma de medicamentos. Se excluyeron pacientes con urocultivo/espermocultivo positivos, litiasis, biopsia y/o cirugía de órganos pélvicos ó cáncer pélvico, y lesiones del snc. Las variables se analizaron mediante Anova y Tukey pos hoc test, 95% ic, usando el software spss 10.1. Resultados: Media de edad 34.23±12.90 años, media del tiempo de evolución 19.58±12.08 meses, sin diferencia estadística en entre grupos. La diferencia de las medias en el promedio de emg (avgemg) del grupo ptns pre vs trans de 0.125 µV y de pre vs 72 horas de 0.171 µV fueron significativas (p<0.05), mientras que en el grupo placebo la diferencia de las medias avgemg de 0.013 µV y 0.006 µV sin diferencia estadística (p>0.05). Conclusiones: El cambio inmediato sobre la mpp que permanece hasta 72 horas después de la ptns, es un posible mecanismo de acción de neuroplasticidad de la neuromodulación del nervio tibial.
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 significantly disrupted EUS fibers and nerve-conduction (VD vs SH-VD group;p < 0.01). Urine leakage disappeared 13 days post-VD (p < 0.001). Structural and functional recovery of EUS neuromuscular circuitry started by day 6 post-VD, but did not fully recover by day 11 post-VD (p > 0.05). TENS significantly decreased the frequency of urine leakage post-VD (days 5–7;p < 0.01). We conclude that rat urinary continence after VD requires 2 weeks to recover, although urethra structure is not fully recovered. TENS facilitated urinary continence recovery after VD. Additional studies are necessary to assess if TENS could be used in postpartum women.
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