Prevention of Obstruction Induced Bladder Damage by Acetylsalycylic Acid

Abstract

Purpose Obstruction induced degeneration of bladder function and structure may be partly due to ischemia that occurs during periods of increased bladder pressure. We investigated what effect administration of acetylsalycylic acid (ASA) to animals with an urethral obstruction has on bladder function and structure. Material and methods A guinea pig model for urethral obstruction was used. Animals were followed with weekly urodynamic investigations. This yielded data on urine flow, bladder pressure, instability, compliance and contractility. Bladder material was obtained at end point and analysed wit a PAS stain for overall-structure and for glycogen accumulation (indicator for ischemia). A group of 8 animals that received ASA during 10 weeks of obstruction was compared to historic groups of obstructed animals (n = 93) and sham operated animals (n = 13). Results Compared to the obstructed group, ASA increased bladder pressure and contractility, prevented the obstruction induced decrease in compliance and had no effect on instability. ASA completely prevented the glycogen accumulation that occurs in obstructed bladders. Conclusions ASA appears to improve the bloodcirculation through the bladder wall in obstructed bladders. The bladder muscle can function aerobically, as indicated by the lack of glycogen accumulation, which is more effective, as witnessed by the increased contractility. The increased pressure does not damage the bladder wall and compliance thus is preserved. Instability still occurs. Our working hypothesis is that in an obstructed bladder the high pressure induces afferent nerves to produce contraction signals directly and also indirectly by ischemia induced damage of the afferent nerves. With ASA the pressure induced signals remain while the signals related to ischemia are absent. Further study into the density of afferent nerves in the bladder wall is in progress to test this hypothesis. Furthermore we will test the effect of a combination of oxybutynin and ASA on bladder function in our model.