Effects of tramadol on rat detrusor overactivity induced by experimental cerebral infarction.

Abstract

Cerebrovascular disease, such as stroke, frequently results in incontinence by reducing suprapontine micturition control. Intraluminal occlusion of the middle cerebral artery (MCA), which produces detrusor overactivity, has been introduced as a useful model of stroke-induced lower urinary tract dysfunction. Recently, the effective analgesic tramadol, was found to possess inhibitory actions on normal rat micturition. The current study aimed to examine the potential effect of tramadol on rat detrusor overactivity due to cerebral infarction. In female Sprague-Dawley rats, cerebral ischemia was induced by occlusion of the MCA and the urinary bladder was catheterised. Three days later, continuous cystometry was performed in awake animals and the effects of tramadol given intravenously were studied. In cerebral infarcted rats, bladder capacity was lower (48+/-9%) and micturition pressure higher (76+/-21%) than in control rats. Tramadol 5 mg x kg(-1) given i.v., increased bladder capacity (59+/-29%) and threshold pressure (47+/-32%) to values similar to those in control rats. However, micturition pressure was not significantly altered. Tramadol induced diuresis in some, but not all, cerebral infarcted rats. Tramadol normalised detrusor overactivity in MCA-occluded rats. The drug might have a treatment potential in patients with detrusor overactivity after stroke.