G Bratslavsky1, B Kogan, R M Levin. 1. Albany College of Medicine, Albany College of Pharmacy and Stratton Veterans Affairs Medical Center, Albany, New York, USA.
Abstract
PURPOSE: Experimental studies have demonstrated that ischemia may induce significant bladder dysfunction. Because multiple causes leading to bladder ischemia also decrease urethral perfusion, we assessed the effect of in vitro ischemia on the contractile responses of the rat bladder and urethra. We evaluated the hypothesis that neurogenic dysfunction in urethral ischemic injury occurs before myogenic dysfunction is present. We also compared contractile responses of the rat bladder and urethra to in vitro ischemia followed by reoxygenation. MATERIALS AND METHODS: Isolated strips of rat bladder detrusor muscle and prostatic urethra were incubated in normal physiological medium and stimulated electrically and chemically. In vitro ischemia was produced by incubating tissue in ischemic medium for 30 or 60 minutes. The maximal tension and maximal rate of tension generated were analyzed digitally before ischemia and after ischemia followed by reoxygenation. RESULTS: We demonstrated that after 30 minutes of ischemia followed by reperfusion the maximal rate of tension generated decreased significantly only in the urethra and only in response to field stimulation. After 60 minutes of ischemia the decrease in urethral contractile responses was greater than the decrease in bladder contractile responses. Ischemia 60 minutes in duration caused a significant decrease in the maximal rate of tension generated as well as maximal tension in the urethra and bladder but only in response to field stimulation. CONCLUSIONS: This experiment demonstrates that the urethra is more sensitive to ischemic injury than the bladder. Our finding may explain the development and symptoms of urinary incontinence secondary to sphincteric damage before bladder dysfunction is present. We also demonstrated that in the bladder and urethra the response to field (neurogenic) stimulation is the most sensitive form of stimulation to ischemia.
PURPOSE: Experimental studies have demonstrated that ischemia may induce significant bladder dysfunction. Because multiple causes leading to bladder ischemia also decrease urethral perfusion, we assessed the effect of in vitro ischemia on the contractile responses of the rat bladder and urethra. We evaluated the hypothesis that neurogenic dysfunction in urethral ischemic injury occurs before myogenic dysfunction is present. We also compared contractile responses of the rat bladder and urethra to in vitro ischemia followed by reoxygenation. MATERIALS AND METHODS: Isolated strips of ratbladder detrusor muscle and prostatic urethra were incubated in normal physiological medium and stimulated electrically and chemically. In vitro ischemia was produced by incubating tissue in ischemic medium for 30 or 60 minutes. The maximal tension and maximal rate of tension generated were analyzed digitally before ischemia and after ischemia followed by reoxygenation. RESULTS: We demonstrated that after 30 minutes of ischemia followed by reperfusion the maximal rate of tension generated decreased significantly only in the urethra and only in response to field stimulation. After 60 minutes of ischemia the decrease in urethral contractile responses was greater than the decrease in bladder contractile responses. Ischemia 60 minutes in duration caused a significant decrease in the maximal rate of tension generated as well as maximal tension in the urethra and bladder but only in response to field stimulation. CONCLUSIONS: This experiment demonstrates that the urethra is more sensitive to ischemic injury than the bladder. Our finding may explain the development and symptoms of urinary incontinence secondary to sphincteric damage before bladder dysfunction is present. We also demonstrated that in the bladder and urethra the response to field (neurogenic) stimulation is the most sensitive form of stimulation to ischemia.