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Changes in bladder and external urethral sphincter function after spinal cord injury in the rat
M N Kruse1, A L Belton, W C de Groat
1Department of Pharmacology, University of Pittsburgh, Pennsylvania 15261.
The American Journal of Physiology
|June 1, 1993
Summary
Spinal cord injury (SCI) causes bladder-sphincter dyssynergia in rats, mimicking human dysfunction. Abnormal external urethral sphincter (EUS) activity impairs bladder emptying, highlighting similarities in voiding deficits after SCI.
Area of Science:
- Neuroscience
- Urology
- Physiology
Background:
- Spinal cord injury (SCI) in humans leads to bladder-sphincter dyssynergia and urinary retention.
- External urethral sphincter (EUS) muscle overactivity during micturition is a key issue in human SCI patients.
Purpose of the Study:
- To investigate if SCI in rats causes similar detrimental effects on micturition as observed in humans.
- To analyze the role of EUS activity patterns during voiding post-SCI in a rat model.
Main Methods:
- Chronic SCI was induced in rats.
- Micturition function, including bladder capacity and residual volume, was assessed under urethane anesthesia.
- Electromyography (EMG) of the EUS was recorded during voiding.
- Neuromuscular blockade was used to suppress EUS activity.
Main Results:
- Rats with chronic SCI exhibited a 15-fold increase in bladder capacity and a 31-fold increase in residual volume.
- SCI rats showed abnormal tonic EUS EMG activity during bladder contractions, unlike the bursting pattern in controls.
- Suppressing EUS activity did not improve voiding in SCI rats and worsened it in controls.
Conclusions:
- Rats and humans display comparable micturition dysfunctions following SCI, including bladder-sphincter dyssynergia.
- Abnormal EUS activity, whether tonic or completely quiescent, is detrimental to bladder emptying.
- Normal bursting EUS activity appears crucial for facilitating bladder emptying during micturition.