Persistent vesical dysfunction is often encountered after long term bladder overdistension caused by urinary retention. Experimentally, acute overdistension has also been implicated in the pathogenesis of the response to partial outlet obstruction. In the present study, we evaluated the expression of iNOS in the partially obstructed rat bladder and presupposed that NO is responsible for the prolonged micturition problem after partial outlet obstruction of the rat bladder. Female Sprague-Dawley rats weighing 150~200g were used. Individual bladders were obtained from unoperated control rats, and from rats at 6, 12, 48, 72 hours, 5 and 7 days after partial urethral obstruction. Total RNA was extracted from each of these tissue. The expression of mRNAs were assessed by Northern blot analysis. The band intensity of the autoradiographs measured by densitometry were compared between the obstructed and control group. The expression of mRNA for iNOS was detected in the control rats. The expression showed a sharp increase at 6 hours (342% increase) after obstruction and returned to normal by 24 hours. In this study, we show that iNOS increases in the rat bladder after operation and these results suggest that overproduction of NO may be a possible mechanism for the prolonged bladder dysfunction after partial bladder outlet obstruction.
Animals ; Blotting, Northern ; Densitometry ; Female ; Humans ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type II* ; Rats* ; Rats, Sprague-Dawley ; RNA ; RNA, Messenger* ; Urethral Obstruction ; Urinary Bladder Neck Obstruction* ; Urinary Bladder* ; Urinary Retention ; Urination