PURPOSE: Our objective was to evaluate the effect of the calcium (Ca2+) channel blocking agent nifedipine on bladder overactivity induced by middle cerebral artery (MCA) occlusion and determine its site of action. MATERIALS AND METHODS: Seven days after implantation of a bladder catheter, a cannula for intracerebroventricular and intrathecal administration was implanted and the left MCA was occluded with 4-0 monofilament nylon thread in male SD rats. Twenty-four hours after the induction of cerebral ischemia, saline was infused into the bladder at a constant rate (200 microL/min.) and cystometrogram was measured in conscious state. Nifedipine was administered intracerebroventricularly (5 microL) or intrathecally (20 microL) at graded doses (0.15 ng.-0.15 microg., 0.15 microg. -1.5 microg., respectively). RESULTS: Bladder capacity in conscious rats was significantly reduced after the left MCA occlusion. Intracerebroventricular administration of nifedipine significantly increased bladder capacity in cerebral infarcted rats but not in sham operated rats. Furthermore there was no significant difference in bladder capacity between before and after intrathecal administration of nifedipine in cerebral infarcted rats. CONCLUSION: These results show that Ca2+ channel blocking agents can operate especially on the supraspinal central nervous system rather than on the spinal system in rats with neurogenic bladder overactivity following cerebral infarction.
PURPOSE: Our objective was to evaluate the effect of the calcium (Ca2+) channel blocking agent nifedipine on bladder overactivity induced by middle cerebral artery (MCA) occlusion and determine its site of action. MATERIALS AND METHODS: Seven days after implantation of a bladder catheter, a cannula for intracerebroventricular and intrathecal administration was implanted and the left MCA was occluded with 4-0 monofilament nylon thread in male SD rats. Twenty-four hours after the induction of cerebral ischemia, saline was infused into the bladder at a constant rate (200 microL/min.) and cystometrogram was measured in conscious state. Nifedipine was administered intracerebroventricularly (5 microL) or intrathecally (20 microL) at graded doses (0.15 ng.-0.15 microg., 0.15 microg. -1.5 microg., respectively). RESULTS: Bladder capacity in conscious rats was significantly reduced after the left MCA occlusion. Intracerebroventricular administration of nifedipine significantly increased bladder capacity in cerebral infarctedrats but not in sham operated rats. Furthermore there was no significant difference in bladder capacity between before and after intrathecal administration of nifedipine in cerebral infarctedrats. CONCLUSION: These results show that Ca2+ channel blocking agents can operate especially on the supraspinal central nervous system rather than on the spinal system in rats with neurogenic bladder overactivity following cerebral infarction.
Authors: Eric Chieh-Lung Chou; Catherine Whitbeck; Jeffrey Herz; Gregory A Demopulos; Robert M Levin Journal: Int Urol Nephrol Date: 2007-02-28 Impact factor: 2.370