Do atherosclerosis and chronic bladder ischemia really play a role in detrusor dysfunction of old age?

To determine whether atherosclerosis-induced chronic pelvic ischemia plays a role in the pathogenesis of aging bladder dysfunction. Old (70 weeks of age), apolipoprotein E gene knockout (APOEKO) mice, known to develop atherosclerosis spontaneously were used. A group of 70-week-old C57B mice were used as controls. The mice were killed and bladder smooth muscle strips obtained for in vitro contractile force determinations. The maximal contractions in response to 110 mM KCl, 10 −5 M bethanechol, and resting muscle tone were compared. The abdominal aortas and iliac arteries were harvested from the mice, and computerized image analysis was used to determine the percentage of surface area of atherosclerosis in each mouse. Although the APOEKO mice had massive atherosclerosis of the abdominal aortas and iliac arteries (lesion surface area ± SEM 15.93% ± 3.02%, n = 4), the control mice (n = 5) had no atherosclerosis at all. No statistically significant difference was found in detrusor function (KCl 0.48 ± 0.11 versus 0.49 ± 0.05, bethanechol 0.11 ± 0.02 versus 0.13 ± 0.04, tone 0.063 ± 0.019 versus 0.07 ± 0.004, respectively) between the APOEKO mice (n = 6) and the control mice (n = 6). Pelvic atherosclerosis caused no statistically significant changes in bladder smooth muscle contractile responses to bethanechol, KCl, or resting tone. The difference between these and previously reported results may have been a result of the more gradual onset of atherosclerosis in our model, which better mimics pelvic organ ischemia in the elderly.