AIMS: To determine whether alpha1-blocker treatment, in chronic bladder outlet obstruction (BOO), influences bladder tissue ischemia. MATERIALS AND METHODS: This prospective study included 60 patients with BOO, of which 40 were under alpha1-blocker medication and 20 without treatment. Patients underwent transurethral resection of the prostate (TURP) or suprapubic prostatectomy (SPP). Ten patients with non-muscle invasive bladder cancer underwent transurethral resection of the bladder tumor and served as the control group. Tissue specimens were immunohistochemically stained for hypoxia inducible factor-1alpha (HIF-1alpha). RESULTS: Bladder tissue from obstructed subjects showed high immunoreactivity to HIF-1alpha. The specimens from the control group, showed no or weak, mainly cytoplasmic immunoreactivity to HIF-1alpha. Patients under alpha -blocker treatment did not differ in the number of HIF-1alpha positive cells compared to subjects with no treatment (median number 86.8 [20-150] and 88.6 [0-175], respectively) (p > 0.05). The lowest bladder pressure at which HIF-1alpha was up regulated, was detected at detrusor pressure Qmax (PdetQmax) = 60 cm H2O. CONCLUSIONS: Treatment with alpha-blockers in obstructed patients considered as non-responders, does not result in HIF-1alpha down regulation, thus bladder continues to be under chronic stress.
AIMS: To determine whether alpha1-blocker treatment, in chronic bladder outlet obstruction (BOO), influences bladder tissue ischemia. MATERIALS AND METHODS: This prospective study included 60 patients with BOO, of which 40 were under alpha1-blocker medication and 20 without treatment. Patients underwent transurethral resection of the prostate (TURP) or suprapubic prostatectomy (SPP). Ten patients with non-muscle invasive bladder cancer underwent transurethral resection of the bladder tumor and served as the control group. Tissue specimens were immunohistochemically stained for hypoxia inducible factor-1alpha (HIF-1alpha). RESULTS: Bladder tissue from obstructed subjects showed high immunoreactivity to HIF-1alpha. The specimens from the control group, showed no or weak, mainly cytoplasmic immunoreactivity to HIF-1alpha. Patients under alpha -blocker treatment did not differ in the number of HIF-1alpha positive cells compared to subjects with no treatment (median number 86.8 [20-150] and 88.6 [0-175], respectively) (p > 0.05). The lowest bladder pressure at which HIF-1alpha was up regulated, was detected at detrusor pressure Qmax (PdetQmax) = 60 cm H2O. CONCLUSIONS: Treatment with alpha-blockers in obstructed patients considered as non-responders, does not result in HIF-1alpha down regulation, thus bladder continues to be under chronic stress.