ArticleAmerican journal of physiology. Renal physiology2010
Pudendal nerve injury reduces urethral outlet resistance in diabetic rats.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- Brain-Derived Neurotrophic Factor Is Indispensable to Continence Recovery after a Dual Nerve and Muscle Childbirth Injury Model.International journal of molecular sciences · 2023Article
- Current and Future Directions of Stem Cell Therapy for Bladder Dysfunction.Stem cell reviews and reports · 2020Review
- Advanced glycation end products facilitate bacterial adherence in urinary tract infection in diabetic mice.Pathogens and disease · 2015Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
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.
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