The Alteration In Bladder Morphology And Function After Acute Urinary Retention And Its Corelation With Active Oxygen Species

Background and Objectives:The acute urinary retention (AUR) is a common and severe complication seen after lower urnary tract obstruction , some surgical treatments, applications of some drugs and cerebrovascular accidents etc.The clinical significance of AUR lies in the severe bladder functions impairment manifested by prolonged bladder function recovery and even inreversible bladder function loss.Unfortunately, no effective treatment is available in the urologist's disposal at present and under many circumstances, urinary drainage is the only option in the hope to let the automatic bladder function recovery. Due to the" lacking appreciation of the pathophysiology of AUR, the clinical index for prognosis is absent which impedes the decision of catheter withdrawl time. There is typical ischemia-reperfusion during AUR/emptying and it has been proved that the ischemia-reperfusion can do great harm to heart , brain and kidney etc, in which the ROS plays a vital role.The ischemia-reperfusion impairment varies among different tissues or organs so it is essential to study the morphological and functional alteration in bladder after acute urinary retention and its corelation with active oxygen.Methods:The AUR experimental model was established and the effect of AUR on the morphological and functional alterations of bladder was observed. All the rats were devided into control group, AUR group and SOD treatment group randomly. The control group were only subjected to cystometry while after cystometry of normal bladder volume, compliance and excitability, the AUR as well as the SOD groups then were treated by double normal volume filling and maintained for 2 hours(acute urinary retention model).On the time scale of 0, 1, 2, 3, 4 hours after emptying, cystometry was performed in the AUR groups. Inthe SOD group, 10 minutes before emptying, 500U SOD was injected into the left cardiac ventricle and the following procedures were the same with the E2 group. After cystometry, the urinary bladders were immediately removed to be subjected to H-E staining, TUNEL staining, XOD and MDA assays.In the C, E0, E2 and SOD groups, the subcellular calcium distribution were observed by electron microscopy.The effects of H2O2 on the cytoplasmic free calcium in cultured detrusor myocytes:A enzymatic dissociation approach was successfully adopted to culture the detrusor myocytes. After loaded by Fluo-4/AM, the real time cytoplasmic free calcium concentrations in detrusor myocytes were obtained by adding H2O2 with varying concentrations to the normal as well as under circumstances of free extracellular calcium and pre calcium channenl blocker treatment cultured detrusor myocytes respectively.Main results and conclusions:1 The first characteristic of AUR/emptying in rat was distinctive tissue layer impairment with conspicuous damage to the mucosa plus submucosa while relatively light damage to the muscular layer and the second was the damage mainly occurred during reperfusion stage.2 AUR/emptying in rat could result in obvious bladder function alterations featured by declining compliance and increasing detrusor excitability.3 The increase of ROS after AUR/emptying plays a pivotal role in the bladder function impairment.4 Application of SOD before emptying could obviously ameliorate the functional alterations of bladde suggesting that antioxidant might be useful in the AUR treatment clinically.5 Addition of H2O2 can induce dose-dependent inhancement of cytoplasmic free calcium concentration in cultured detrusor myocytes.6 The increase of cytoplasmic free calcium concentration in cultured detrusor myocytes by H2O2 addition takes action maily by virture of extracellular calcium influx through calcium channel.7 The calcium channel blockers Nimodipine and Verapamil can inhibite thecytoplasmic free calcium increase resulted from H2O2 addition indicating that in the clinical practice of AUR management; the calcium inhibitors should be applied to prevent bladder damage secondary to the extracellular calcium influx before emptying the bladder.