Antioxidants, free radical scavengers or substances inhibiting I/R injury may reduce bladder damages caused by BOO or overdistention. As any organ in the body, the urinary bladder needs an adequate blood supply to obtain oxygen and nutrition to function normally. Ischemia with the accompanied Rapamycin manufacturer hypoxia would expect to impair bladder function. Cumulated evidences have demonstrated that ischemia, hypoxia and ischemia/reperfusion (I/R), with the accompanying generation of reactive oxygen/nitrogen species, are important etiologic factors in obstructive
bladder dysfunction.1,2 The present paper reviews and summarizes the effects of ischemia and hypoxia on the energy metabolism and contractile PI3K inhibitor function of the urinary bladder. I/R injury on the bladder and its role in chronic bladder outlet obstruction and acute overdistention are further reviewed. Chronic partial ischemia of the bladder has been shown to impair bladder function. Gill et al. have shown that bladder ischemia induced by ligation of the vesical artery impaired contractile responses of the detrusor strips.3 Lin el al. found that chronic ischemia of the bladder resulted in a decrease of bladder compliance with a reduction in the contractility of the whole bladder.4
Lit et al. further demonstrated that chronic ischemia deranged glucose metabolism of the detrusor with a reduction in glycogen content and an increase CYTH4 in anaerobic metabolism, resulting in a much lower production of high-energy molecules.5 Using an atherosclerosis rabbit model, a recent study also demonstrated that chronic ischemia of the urinary bladder resulted in mitochondrial injury, fibrosis, microvasculature damage and neurodegeneration.6 Lin et al. have demonstrated that urinary bladder blood flow was reduced by outlet obstruction
and the reduction in blood flow was associated with decreased tissue level of high-energy phosphates, adenosine triphosphate (ATP) and creatine phosphate.7 They further showed that the BOO-induced blood flow reduction could be recovered gradually after relieving outlet obstruction and was in parallel with the recovery of energy producing-related mitochondrial enzyme activity and energy producing capability of the bladder.8,9 During bladder emptying, the increased intra-wall tension results in blood vessel compression, decreased blood flow and tissue hypoxia. This occurs in normal bladders; nevertheless, this phenomenon is significantly exaggerated in the obstructed hypertrophied bladder.2,10 Under conditions of increased oxidative stress, cellular and subcellular membranes become subject to attacks when the generation of free radicals outweighs the system’s ability to eliminate.
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