Introduction: BTX-A has been proven effective in the treatment of neurogenic BO. The goal of this project was to assess the effects of BTX-A on BO in the rat model of CYP-induced cystitis and bladder outflow obstruction.
Methods: Under general anesthesia through a lower midline abdominal incision, 5 units of BTX-A (study group) or vehiculum (controls) divided into 10 injections was injected into the wall of the urinary bladder of adult female Wistar rats. Three weeks following the BTX-A injection, PE-50 tubing was implanted into the bladder dome and tunneled subcutaneously to the back of the neck. Following the 72 hour recovery period, the animals were injected with CYP (150 mg/kg i.p.). Cystometrograms were performed in the conscious, freely moving rats 4 or 48 hours after the CYP treatment. In another group of rats, six weeks following the creation of the bladder outflow obstruction, the bladder overactivity was confirmed with a conscious cystometrogram. Animals who developed bladder overactivity received an injection of 5 units of BTX-A divided into five injections into the wall of urinary bladder. Following this treatment, a cystometrogram was repeated on the same animal three times in weekly intervals.
Results: Four hours following the CYP injection in the BTX-A-treated animals, the bladder capacity was 4.1-fold higher, filling pressure was 2.8-fold lower when compared to the control, BTX-A-untreated animals. The micturition pressure remained unchanged. In the BTX-A-treated animals that were studied 48 hours following CYP injection the bladder capacity was 4-fold higher, and the filling pressure was 3.1-fold lower and the micturition pressure was reduced by 40% compared to controls. In the animals with BOO, the most significant changes in intravesical pressure were noted three weeks following the BTX-A injection. Filling pressure decreased 2.2-fold and threshold pressure decreased 2.2-fold. The number and amplitude of non-voiding bladder contractions decreased significantly.
Conclusion: Injection of the BTX-A into the wall of the urinary bladder in the rat model of CYP-induced cystitis resulted in a significant increase in bladder capacity and a reduction of the filling pressure. BTX-A reduced bladder overactivity in a rat model of BOO. This suggests that BTX-A has a potential as a treatment of bladder overactivity in patients with non-neurogenic bladder dysfunction.

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