Saito M, Wada K, Kamisaki Y, Miyagawa I
Department of Urology, Faculty of Medicine, Tottori University, Yonago, Japan.
Life Sci. 1998;62(11):PL149-56. doi: 10.1016/s0024-3205(98)00026-5.
Because there are increasing evidences that nitric oxide (NO) plays important roles in ischemia-reperfusion injury in several systems, we investigated the role of NO in ischemia-reperfusion injury of the rat urinary bladder. Rat abdominal aorta was clamped with a small clip to induce ischemia-reperfusion injury in the rat bladder dome. In functional studies, contractile responses to carbachol were cumulatively measured after the urinary bladder was treated with various duration (0, 30, 60, and 90 min) of ischemia. The injury of rat bladder functioning was dependent on ischemic periods. Significant decreases in the Emax (maximum contractile response) values were observed in the bladder subjected to 60 or 90 min ischemia. Furthermore, the subsequent 30 min reperfusion caused additional damages of the contractile response in bladder muscles. To investigate the role of NO in the ischemia (30 min)-reperfusion (30 min) injury, NG-nitro-L-arginine methylester (L-NAME) was injected intraperitoneally 30 min before the ischemia. Treatment of L-NAME (30 and 100 mg/kg) partly but significantly prevented the reduction contractile responses to carbachol of the rat bladder dome. In histological studies, the ischemia-reperfusion caused infiltration of leukocytes and rupture of microcirculation in the regions of submucosa and smooth muscle without a corresponding sloughing of mucosal cells. The histological damages were also prevented by treatment with L-NAME. Therefore, these data suggested that ischemia-reperfusion of the urinary bladder may result in dysfunction of the contractile response to autonomic nervous system and that nitric oxide may act as a cell/tissue damaging agent in ischemia-reperfusion injury.
