Abstract
Spinal cord injury (SCI) can lead to detrusor overactivity and detrusor-sphincter dyssynergia, which result in inefficient voiding and bladder wall tissue remodeling such as hypertrophy and fibrosis. However, no effective modality for controlling the bladder remodeling is available. Phosphodiesterase type 5 (PDE5) inhibitors and alpha1-adrenoceptor (α1-AR) antagonists are used for the treatment of male lower urinary tract symptoms with benign prostatic hyperplasia.
In animal study, PDE5 inhibitor or α1A/D-AR antagonist treatment suppressed the bladder fibrosis after SCI. PDE5 inhibitor might increases the blood flow and prevents bladder ischemia, resulting in the reducing the load in storage state and the suppressing of bladder fibrosis after SCI. Relaxing the bladder neck and proximal urethra after α1-AR antagonist treatment might decrease the resistance to urine flow from detrusor–sphincter dyssynergia and residual urine volume reduce the load of the bladder wall during both of voiding and storage states. Therefore, treatment with PDE5 inhibitors and α1A/D-AR antagonists could be effective for neurogenic lower urinary tract dysfunction including bladder remodeling after SCI.
