EFFECT OF ISCHEMIA-REPERFUSION ON CONTRACTILE FUNCTION OF RAT URINARY-BLADDER - POSSIBLE ROLE OF NITRIC-OXIDE

Because there are increasing evidences that nitric oxide (NO) plays im portant roles in ischemia-reperfusion injury in several systems, we in vestigated the role of NO in ischemia-reperfusion injury of the rat ur inary bladder. Rat abdominal aorta was clamped with a small clip to in duce ischemia-reperfusion injury in the rat bladder dome. In functiona l studies, contractile responses to carbachol were cumulatively measur ed after the urinary bladder was treated with various duration (0, 30, 60, and 90 min) of ischemia. The injury of rat bladder functioning wa s dependent on ischemic periods. Significant decreases in the E-max (m aximum contractile response) values were observed in the bladder subje cted to 60 or 90 min ischemia. Furthermore, the subsequent 30 min repe rfusion caused additional damages of the contractile response in bladd er muscles. To investigate the role of NO in the ischemia (30 min)-rep erfusion (30 min) injury, N-G-nitro-L-arginine methylester (L-NAME) wa s injected intraperitoneally 30 min before the ischemia. Treatment of L-NAME (30 and 100 mg/kg) partly but significantly prevented the reduc tion contractile responses to carbachol of the rat bladder dome. In hi stological studies, the ischemia-reperfusion caused infiltration of le ukocytes and rupture of microcirculation in the regions of submucosa a nd smooth muscle without a corresponding sloughing of mucosal cells. T he histological damages were also prevented by treatment with L-NAME. Therefore; these data suggested that ischemia-reperfusion of the urina ry bladder may result in dysfunction of the contractile response to au tonomic nervous system and that nitric oxide may act as a cell/tissue damaging agent in ischemia-reperfusion injury. (C) 1998 Elsevier Scien ce Inc.