Results: During cystometry with acetic acid the interval between bladder contractions was shorter and maximum bladder contraction pressure was higher in the control group compared with results obtained using physiological saline but such differences were not seen in the Eviprostat group. Plasma adrenaline and noradrenaline were lower

in the Eviprostat group than the control group but no difference Entrectinib concentration in blood pressure was observed. Urinary adenosine triphosphate was higher in the 2 groups than before stimulation but the increase was smaller in the Eviprostat group than in the control group.

Conclusions: These results suggest that Eviprostat acts to maintain low catecholamine and also inhibit pathological bladder activity by decreasing adenosine triphosphate release from the bladder.”
“Purpose: We hypothesized that transection of the pubo-urethral ligament in the female rat would cause stress urinary incontinence, as indicated

by decreased leak point pressure. We created a novel model of pubo-urethral ligament deficiency in the rat and validated our model through comparison with an established model of stress urinary incontinence.

Materials and Methods: find more A total of 21 female age matched Sprague-Dawley rats (Harlan, Indianapolis, Indiana) were randomly assigned to 5 groups, including pubo-urethral ligament transection or sham pubo-urethral ligament transection. with leak point pressure measured 4 days (groups 1 and 2) or 10 days (groups 3 and 4) postoperatively and bilateral pudendal nerve transection. with leak point pressure measured 4 days postoperatively (group 5). Leak point pressure was measured in all groups via a suprapubic catheter. The Wilcoxon signed rank test was used AZD6738 to evaluate differences between the groups.

Results: Leak point pressure was significantly decreased in the pubo-urethral ligament transection groups compared to that

in the sham treated groups after 4 days (mean +/- SEM 16.3 cm +/- 2.74 vs 36.6 +/- 8.39 cm H2O, p < 0.00001), although it was no different from that in the pudendal nerve transection group (14.5 +/- 1.06 cm H2O, p < 0.44). Ten days after surgery leak point pressure remained significantly lower in the pubo-urethral ligament transection groups compared to that in the sham treated groups (17.6 +/- 6.36 vs 31.2 +/- 5.14 cm H2O, p < 0.00001), indicating the durability of pubo-urethral ligament transection for inducing stress urinary incontinence in female rats.

Conclusions: Our results demonstrate that deficiency of the pubo-urethral ligament in the female rat induces stress urinary incontinence comparable to that in a previously established model of pudendal nerve transection. induced stress urinary incontinence.