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¹ Department of Urology, ² Department of Medical Research, ³ Department of Physiology, ⁵ Department of Pathology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan ⁴ Department of Basic and Pharmaceutical Sciences, Albany College of Pharmacy, Albany, NY, USA

We explored whether hypoxic preconditioning minimizes oxidative injury induced by overdistension/emptying in the rat bladder. For hypoxic preconditioning, female Wistar rats were placed in a hypobaric chamber (380 Torr) 15 h day^-1 for 28 days. Overdistension was induced by infusion of two times the threshold volume of saline into the bladder and was maintained for 1 or 2 h, followed by drainage/emptying. During overdistension (ischaemia) and emptying (reperfusion) periods, a bursting increase of reactive oxygen species (ROS) from the bladder was originated from the large numbers of infiltrating leucocytes and scattered resident cells, including urothelial, submucosal, and smooth muscle cells. ROS impaired the voiding function by a reduction of bladder afferent and efferent nerve activity and bethanecol- or ATP-induced detrusor contraction. ROS enhanced pro-apoptotic mechanisms, including increases in the Bax/Bcl-2 ratio, CPP32 expression, and poly(ADP-ribose) polymerase (PARP) fragments with subsequent apoptotic cell formation in the insulted bladders. Hypoxia preconditioning up-regulated Bcl-2 expression in the bladder and significantly reduced the levels of ROS and apoptosis detected in the overdistension/emptying bladders and preserved partial voiding function. Bcl-2 up-regulation by hypoxia preconditioning contributes protection against overdistension/emptying-induced oxidative stress and injury in the bladder.

(Received 30 September 2003; accepted after revision 5 November 2003; first published online 7 November 2003)
Corresponding author C.-T. Chien: No. 7, Chung-Shan S. Road, Department of Medical Research, National Taiwan University Hospital, Taipei, Taiwan, ROC.  Email: ctchien{at}ha.mc.ntu.edu.tw

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