Objectives: To determine whether external urethral sphincter (EUS) relaxation induced by alpha-bungarotoxin, a highly selective neuromuscular junction blocking agent, could ameliorate voiding dysfunction after spinal cord injury (SCI) in rats.
Methods: The effects of intravenous alpha-bungarotoxin (333 microg/kg) were evaluated during cystometry in decerebrate, unanesthetized female Sprague-Dawley rats (250 to 300 g) with spinal cords chronically transected at T7-9 (n = 7) or with normal spinal cords (NSC) (n = 7). Parameters measured included voided volume (VV), residual volume (RV), volume threshold for inducing micturition (VT), voiding efficiency (VE), micturition pressure (MP), pressure threshold for inducing micturition (PT), bladder contraction duration (BCD), and compliance (CP).
Results: In SCI rats, treatment with alpha-bungarotoxin improved voiding. The toxin increased VE (31%) and reduced RV (42%), MP (52%), BCD (14%), and VT (31%). VV, PT, and CP were not altered. In NSC rats, alpha-bungarotoxin decreased VE (23%), increased RV (63%), and decreased MP (36%), VV (38%), and VT (20%) but did not change BCD and CP.
Conclusions: The results of our study demonstrated that alpha-bungarotoxin improved voiding in SCI rats by reducing urethral outlet resistance. However, in NSC rats, the toxin reduced voiding, probably by suppressing high-frequency phasic sphincter activity, necessary for efficient urine elimination in normal animals. The present results provide further support for the view that drugs that depress striated muscle activity can be useful in the treatment of voiding dysfunction after SCI.