Detrusor contractility to parasympathetic mediators is differentially altered in the compensated and decompensated states of diabetic bladder dysfunction

摘要

Diabetic bladder dysfunction (DBD) affects up to 50 of all patients with diabetes, characterized by symptoms of both overactive and undcractive bladder. Although most diabetic bladder dysfunction studies have been performed using models with type I diabetes, few have been performed in models of type 2 diabetes, which accounts for -90 of all diabetic cases. In a type 2 rat model using a high-fat diet (HFD) and two low doses of streptozotocin (STZ), we examined voiding measurements and functional experiments in urothelium-denuded bladder strips to establish a timeline of disease progression. We hypothesized that overactive bladder symptoms (compensated state) would develop and progress into symptoms characterized by underactive bladder (decompensated state). Our results indicated that this model developed the compensated state at I wk after STZ and the decompensated state at 4 mo after STZ administration. Diabetic bladders were hypertrophied compared with control bladders. Increased volume per void and detrusor muscle contractility to exogenous addition of caibachol and ATP confirmed the development of the compensated state.