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  4. Early Detrusor Application of Botulinum Toxin A Results in Reduced Bladder Hypertrophy and Fibrosis after Spinal Cord Injury in a Rodent Model

Early Detrusor Application of Botulinum Toxin A Results in Reduced Bladder Hypertrophy and Fibrosis after Spinal Cord Injury in a Rodent Model

Toxins, 2022 · DOI: 10.3390/toxins14110777 · Published: November 10, 2022

UrologyPharmacologyNeurology

Simple Explanation

Following spinal cord injury (SCI), pathological reflexes develop that result in altered bladder function and sphincter dis-coordination, with accompanying changes in the detrusor. In a rodent model of contusion SCI, we examined the effect of early bladder chemodenervation with botulinum toxin A (BoNT-A) on bladder histopathology and collagen deposition. Detrusor chemodenervation soon after SCI appears to preserve bladder tissue integrity by reducing the development of detrusor fibrosis and hypertrophy associated with SCI.

Study Duration
8 weeks
Participants
Adult female Long Evans rats
Evidence Level
Not specified

Key Findings

  • 1
    BoNT-A injected bladders of SCI rats weighed significantly less than saline injected bladders of SCI rats.
  • 2
    SCI + BoNT-A animals had significantly thinner bladder walls compared to SCI + saline animals.
  • 3
    SCI + BoNT-A animals had collagen organization in the bladder walls similar to that of uninjured animals.

Research Summary

Following spinal cord injury (SCI), pathological reflexes develop that result in altered bladder function and sphincter dis-coordination, with accompanying changes in the detrusor. In a rodent model of contusion SCI, the effect of early bladder chemodenervation with botulinum toxin A (BoNT-A) on bladder histopathology and collagen deposition was examined. Detrusor chemodenervation soon after SCI appears to preserve bladder tissue integrity by reducing the development of detrusor fibrosis and hypertrophy associated with SCI.

Practical Implications

Clinical Potential

Early use of intradetrusor injection of BoNT-A for patients with SCI may serve as a prophylaxis against the most severe complications of neurogenic bladder.

Mechanism Elucidation

Further studies are needed to define the subcellular mechanisms of tissue preservation to fully exploit this method for preserving bladder health.

Treatment Optimization

Additional research is required to determine the full therapeutic window, optimal dosing, and distribution of BoNT-A to achieve maximal tissue preservation.

Study Limitations

  • 1
    Histological analysis only; functional cystometry is needed to examine effects on bladder compliance and function.
  • 2
    Inability to define the subcellular mechanisms of tissue preservation.
  • 3
    Mechanism of action not defined in this study.

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