ArticleInternational urogynecology journal2017
Impaired contraction and decreased detrusor innervation in a female rat model of pelvic neuropraxia.
Article in International urogynecology journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Omental pedicle transposition for neuropathic stress urinary incontinence: a urodynamic evaluation.Open veterinary journal · 2026Article
- Transcriptomics Reveals Molecular Features of the Bilateral Pelvic Nerve Injury Rat Model of Detrusor Underactivity.Biomolecules · 2023Article
- Bone marrow mesenchymal stem cells therapy on bilateral pelvic nerve crush-induced voiding dysfunction in rats.International urogynecology journal · 2022Article
- Correlation Between Nitric Oxide and Urodynamics in Men With Bladder Outlet Obstruction.International neurourology journal · 2022Article
- Dysfunctional voiding behavior and impaired muscle contractility in a rat model of detrusor underactivity.Neurourology and urodynamics · 2021Article
- Establishment of animal model manifested as bladder neurogenic changes generated by bilateral pelvic nerve injury in male rats.International urology and nephrology · 2021Article
- Pathophysiology of the underactive bladder.Investigative and clinical urology · 2017Review
- Pathogenesis evidence from human and animal models of detrusor underactivity.Tzu chi medical journalReview
- Amniotic Fluid Stem Cells Improve Rat Bladder Dysfunction After Pelvic Nerve Transection.Cell transplantationArticle
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
Abstract
introduction and hypothesisBilateral pelvic nerve injury (BPNI) is a model of post-radical hysterectomy neuropraxia, a common sequela. This study assessed the time course of changes to detrusor autonomic innervation, smooth muscle (SM) content and cholinergic-mediated contraction post-BPNI.
methodsFemale Sprague-Dawley rats underwent BPNI or sham surgery and were evaluated 3, 7, 14, and 30 days post-BPNI (n = 8/group). Electrical field-stimulated (EFS) and carbachol-induced contractions were measured. Gene expression was assessed by qPCR for muscarinic receptor types 2 (M2) and 3 (M3), collagen type 1α1 and 3α1, and SM actin. Western blots measured M2 and M3 protein expression. Bladder sections were stained with Masson's trichrome for SM content and immunofluorescence staining for nerve terminals expressing vesicular acetylcholine transporter (VAChT), tyrosine hydroxylase (TH), and neuronal nitric oxide synthase (nNOS).
resultsBilateral pelvic nerve injury caused larger bladders with less SM content and increased collagen type 1α1 and 3α1 gene expression. At early time points, cholinergic-mediated contraction increased, whereas EFS-mediated contraction decreased and returned to baseline by 30 days. Protein and gene expression of M3 was decreased 3 and 7 days post-BPNI, whereas M2 was unchanged. TH nerve terminals surrounding the detrusor decreased in all BPNI groups, whereas VAChT and nNOS terminals decreased 14 and 30 days post-BPNI.
conclusionsBilateral pelvic nerve injury increased bladder size, impaired contractility, and decreased SM and autonomic innervation. Therapeutic strategies preventing nerve injury-mediated decline in neuronal input and SM content may prevent the development of a neurogenic bladder and improve quality of life after invasive pelvic surgery.
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Registered trials
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