急性尿潴留大鼠膀胱组织黄嘌呤氧化还原酶活性变化及其意义

目的探讨在急性尿潴留时大鼠膀胱组织黄嘌呤氧化还原酶(xanthine oxidoreductase,XOD)活性变化的意义.方法以2倍于正常膀胱容量充盈膀胱2 h建立大鼠急性尿潴留模型.分别于充盈2 h及排空后1、2、3、4 h检测膀胱功能及膀胱组织中XOD活性及脂质过氧化产物丙二醛(malondialdebde,MDA)含量;并观察超氧化物歧化酶(superoxide dismutase,SOD)对膀胱的保护作用.结果急性尿潴留期膀胱不稳定性收缩频率无显著改变,而排空后其不稳定性收缩频率增加.XOD活性在尿潴留期增高,排空后1 h活性降低,排空后2 h再次升高,随后逐渐降至正常.MDA在尿潴留期轻度增高,排空后早期明显增高,4 h后接近正常对照组水平.SOD治疗后逼尿肌不稳定性收缩频率、XOD活性及MDA含量与排空后2 h比较显著降低(P＜0.01,0.05).结论AUR时黄嘌呤氧化还原酶活性变化特征呈双相性改变.提示AUR后膀胱再灌注损害中内源性活性氧可能起诱导、促进炎症损害作用,外源活性氧在急性尿潴留排空后膀胱功能损害中可能起重要作用.

Changes of XOD activity induced by acute urinary retention in rats

Objective To study the changes of xanthine oxidoreductase(XOD) activity induced by acute urinary retention(AUR) in rats and its significance.Methods Twenty-eight female Wistar rats were used to establish acute urinary retention model by filling bladder with 2fold bladder volume and maintaining for 2 h.Cystometry,XOD activity and malondialdehyde(MDA) concentration assays were performed at the end of over-distention and 1 h,2 h,3 h,4 h after emptying respectively.The effect of superoxide dismutase(SOD) was observed by injecting 500 U SOD into the left cardiac ventricle of 7 model rats 10 min before emptying.Another 7 rats were filled with normal bladder volume as controls and underwent filling cystonetry.Results The frequency of detrusor over-activity increased more obviously after emptying than during over-distention.XOD activity increased obviously during over-distention period as compared to controls,reduced 1 h after emptying,then increased again 2 h after emptying,finally down to normal level slowly.The concentration of MDA increased during over-distention and early period after emptying and peaked at 1 h after emptying and then recovered slowly.After SOD treatment,the frequency of detrusor over-activity,XOD activity and MDA concentration reduced as compared with that in model rats 2 h after emptying(P<0.01).Conclusion The XOD activity is characterized of diphasic changes,which indicates that exogenous reactive oxygen species(ROS) may play an important role in bladder damage after AUR,while endogenous ROS may induce inflammation and reperfusion injury after AUR.