While the prevalence of the very final stages of BOO is not as high as in previous generations, thanks to improvements in medical and surgical management, the majority of the clinical burden can still be attributed to chronic effects of this disorder. Over the course of several years or decades this disorder can progress to a chronic stage characterized by bladder decompensation with urinary retention and overflow incontinence. In patients with BPH the obstruction slowly worsens over time, causing a progression from initial obstructive symptoms (e.g., urinary hesitancy) to early stage irritative problems such as urinary frequency that can be quite bothersome to patients. However, by far the most common cause of BOO is benign prostatic hyperplasia (BPH) ( 19), which is both chronic and progressive. Acute insults include blood clot retention and certain medication, while more chronic phenomena include urethral strictures and organ prolapse. Together the results suggest a critical role for NLRP3 in mediating bladder decompensation and nerve density during chronic BOO.īladder outlet obstruction (BOO) can arise from both acute and chronic etiologies. Finally, a reduction in nerve density was apparent with BOO and attenuated with glyburide. Moreover, there was a dramatic decrease in voiding efficiency in the chronic BOO rats, which was prevented with glyburide treatment. However, postvoid residual volumes were greatly increased in BOO rats while BOO+gly rats were not different than controls. No difference in frequency or voided volume was detected. Voiding pressures were increased, and flow rates decreased in BOO and BOO+gly groups, demonstrating physical obstruction. BOO greatly enhanced bladder weights and inflammation, while inflammation was prevented by glyburide. After 42 days, bladder weight, inflammation (Evans blue), urodynamics, and nerve density were measured. Four groups were examined: control, sham-operated, BOO, or BOO+gly (glyburide an NLRP3 inhibitor). Currently, we have examined rat bladder function and nerve densities after chronic BOO to determine whether NLRP3 plays a role in the decompensation at this stage. However, as BOO progresses, the bladder may become decompensated with an increase in postvoid residual volume and decreased voiding efficiency. We have previously shown that BOO triggers inflammation, reduced bladder nerve density and increased fibrosis via activation of the NLRP3 inflammasome in an acutely obstructed (12-day) rat model. Over time, inflammation leads to decreased bladder nerve density and increased fibrosis, responsible for eventual decompensation and irreversibility. Acutely, obstruction triggers inflammation that drives bladder dysfunction. Bladder outlet obstruction (BOO) leads to progressive voiding dysfunction.
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