Sacral nerve electrical stimulation (SNES) ameliorates bladder dysfunction and detrusor fibrosis in early-stage spinal cord injury: A randomized controlled experimental study in rats.

This study evaluated the therapeutic effects of sacral nerve electrical stimulation (SNES) targeting the L6-S1 spinal nerves on neurogenic bladder dysfunction following spinal cord injury (SCI). Using a randomized controlled design, 80 female Sprague-Dawley rats were divided into four groups: sham surgery, complete T9 spinal cord transection (SCI model), SCI with electrode implantation only (control), and SCI with active SNES (3-5 Hz, 3-5 V daily for 4 weeks). Bladder function was assessed through urodynamics, while detrusor fibrosis was examined using histological and ultrastructural analyses. The SCI model group demonstrated significant urodynamic impairments compared to sham controls, including increased leak point pressure (43.15 ± 1.37 vs 25.52 ± 1.29 cmH2O) and decreased bladder capacity (1.52 ± 0.21 vs 4.21 ± 0.72 mL) and compliance (0.21 ± 0.14 vs 0.42 ± 0.26 mL/cmH2O; all P < 0.01). SNES treatment substantially reversed these abnormalities (P < 0.01 vs SCI group), restoring parameters to near-normal levels. Histological examination revealed that SNES significantly reduced collagen deposition (types I and III) in detrusor muscle compared to untreated SCI animals (P < 0.05). Transmission electron microscopy showed preserved mitochondrial structure in SNES-treated animals, contrasting with the cellular vacuolization observed in SCI controls. These results demonstrate that early intervention with SNES at the L6-S1 level can effectively mitigate both functional and structural bladder impairments following SCI. The treatment improved urodynamic parameters while reducing fibrotic changes in detrusor muscle, suggesting its potential as a species-specific neuromodulation strategy for neurogenic bladder. This study provides experimental evidence supporting further investigation of sacral-level neuromodulation for SCI-related bladder dysfunction.