泌尿科YU, HONG-JENGHONG-JENGYUCHIEN, CHIANG-TINGCHIANG-TINGCHIENLAI, YU-JENYU-JENLAILAI, MING-KUENMING-KUENLAICHEN, CHAU-FONGCHAU-FONGCHENROBERT M. LEVINHSU, SU-MINGSU-MINGHSU余宏政鄭劍廷賴怡君賴明坤陳朝峰許世明2009-01-162018-07-112009-01-162018-07-112004http://ntur.lib.ntu.edu.tw//handle/246246/97156We 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 for 28 days. Overdistension was in-duced by infusion of two times the threshold volume of saline into the bladder and was main- tained for 1 or 2 h, followed by drainage/emptying. During overdistension (ischemia) and emptying (reperfusion) periods, a bursting increase of reactive oxygen species ( ROS) from the bladder was originated from the large numbers of infiltrating leukocytes 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 acetylcholine- or ATP-induced detrusor contraction. ROS enhanced pro-apoptotic mechanisms, including in-creases in the Bax/Bcl-2 ratio, CPP32 expression, and PARP fragments with subsequent apop- totic cell formation in the insulted bladders. Hypoxia preconditioning upregulated Bcl-2 ex-pression in the bladder and significantly reduced the levels of ROS and apoptosis detected in the overdistension/emptying bladders and preserved partial voiding function. In conclusion, Bcl-2 upregulation by hypoxia preconditioning contributes protection against overdisten-sion/emptying-induced oxidative stress and injury in the bladder.en-USHypoxia preconditioningBladder overdistensionOxidative s