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並列摘要


Partial bladder outlet obstruction (PBOO) in males is mostly caused by benign prostatic hyperplasia. PBOO induces significant alterations in the morphology and physiology of the urinary bladder wall and also results in an impaired ability of the urinary bladder to store and empty urine. Much of our current knowledge is based on animal experiments, and species differences may be a problem when extrapolating these animal findings to the human situation. The primary bladder dysfunction associated with PBOO is a decreased ability to sustain bladder contractions during the voiding phase of the micturation cycle. In animal model, bladder dysfunction and alterations of the mechanistic steps involve detrusor smooth muscle (DSM) contractility. Generally, in response to PBOO, the DSM undergoes compensatory hypertrophy to produce the increased force necessary to expel urine against an obstruction. Besides altering contractile proteins in DSM, PBOO also induces a change of regulatory proteins such as Rho-kinase and protein kinase C. In addition to the impaired ability to empty urine, PBOO is frequently accompanied by non-voiding contractions which can lead to clinical symptoms such as urinary frequency, urgency, and nocturia. Non-voiding contractions could result from a hypersensitivity of the contractile system and/or a reduced sensitivity of the relaxant system. The impairment of β-adrenergic relaxation of bladder smooth muscle and the enhancement of a-adrenergic contraction in PBOO are addressed in this review. Cyclic ischemia and reperfusion (I/R) changes are major etiologic factors in the progression of bladder dysfunction in PBOO. These changes are directly associated with a decrease in energy produced by oxidative phosphorylation in mitochondrial electron transport chain. Furthermore, defects in this chain lead to the generation of a significant quantity of reactive oxygen species in addition to cell apoptosis. Antioxidant agents and mitochondrial respiratory chain coenzyme have been shown to decrease PBOO-induced I/R damage to the bladder.

並列關鍵字

bladder obstruction ischemia overactivity

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