Minoru Miyazato1, Takeya Kitta2, Yasuhiro Kaiho2, Takuma Oshiro3, Seiichi Saito3, Michael B Chancellor4, William C de Groat5, Naoki Yoshimura6. 1. Department of Urology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan; Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Electronic address: miyaz929@med.u-ryukyu.ac.jp. 2. Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. 3. Department of Urology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan. 4. Department of Urology, Oakland University William Beaumont School of Medicine, Royal Oak, Michigan. 5. Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. 6. Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Abstract
PURPOSE: We investigated the effect of duloxetine, a norepinephrine and serotonin reuptake inhibitor, on the sneeze induced continence reflex and on bladder function in rats with cerebral infarction. MATERIALS AND METHODS: Using urethane anesthesia the effect of duloxetine (1 mg/kg intravenously) on the amplitude of urethral responses during sneezing as well as urethral baseline pressure at the mid urethra was evaluated in normal female adult rats and cerebral infarction rats. Tilt leak point pressure was also measured. In normal and cerebral infarction rats continuous cystometry was evaluated before and after duloxetine injection. RESULTS: In cerebral infarction rats urethral baseline pressure was 43% lower than in normal rats but the amplitude of urethral responses during sneezing did not differ in the 2 groups. Duloxetine increased the amplitude of urethral responses during sneezing and urethral baseline pressure by 31% and 21%, respectively, in normal rats but did not affect either in cerebral infarction rats. Also, in cerebral infarction rats leak point pressure was 29% lower compared with normal rats. Duloxetine increased leak point pressure in normal rats but not in cerebral infarction rats. Cerebral infarction reduced intercontraction intervals without affecting the amplitude of bladder contractions compared with normal rats. Duloxetine prolonged intercontraction intervals in cerebral infarction rats but not in normal rats. CONCLUSIONS: These results suggest that cerebral infarction induces not only bladder overactivity but also stress urinary incontinence, which may account for mixed incontinence in patients with cerebral infarction. After cerebral infarction duloxetine reduced bladder overactivity but failed to enhance active urethral closure mechanisms during sneezing, suggesting that disorganization of the brain network after cerebral infarction might influence the effect of duloxetine on lower urinary tract function.
PURPOSE: We investigated the effect of duloxetine, a norepinephrine and serotonin reuptake inhibitor, on the sneeze induced continence reflex and on bladder function in rats with cerebral infarction. MATERIALS AND METHODS: Using urethane anesthesia the effect of duloxetine (1 mg/kg intravenously) on the amplitude of urethral responses during sneezing as well as urethral baseline pressure at the mid urethra was evaluated in normal female adult rats and cerebral infarctionrats. Tilt leak point pressure was also measured. In normal and cerebral infarctionrats continuous cystometry was evaluated before and after duloxetine injection. RESULTS: In cerebral infarctionrats urethral baseline pressure was 43% lower than in normal rats but the amplitude of urethral responses during sneezing did not differ in the 2 groups. Duloxetine increased the amplitude of urethral responses during sneezing and urethral baseline pressure by 31% and 21%, respectively, in normal rats but did not affect either in cerebral infarctionrats. Also, in cerebral infarctionrats leak point pressure was 29% lower compared with normal rats. Duloxetine increased leak point pressure in normal rats but not in cerebral infarctionrats. Cerebral infarction reduced intercontraction intervals without affecting the amplitude of bladder contractions compared with normal rats. Duloxetine prolonged intercontraction intervals in cerebral infarctionrats but not in normal rats. CONCLUSIONS: These results suggest that cerebral infarction induces not only bladder overactivity but also stress urinary incontinence, which may account for mixed incontinence in patients with cerebral infarction. After cerebral infarctionduloxetine reduced bladder overactivity but failed to enhance active urethral closure mechanisms during sneezing, suggesting that disorganization of the brain network after cerebral infarction might influence the effect of duloxetine on lower urinary tract function.
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