[Quantitative electromyographic analysis of the human external urethral sphincter: effect of alpha-adrenergic agents]

External urethral sphincter electromyography (EMG) during bladder filling was quantitatively analysed using automatic decomposition electromyography (ADEMG). These include 7 normal volunteers, 7 patients with outlet obstruction, 9 with sphincter dyssynergia, and 7 with pelvic nerve injury (PNI). Recruited number of participated motor unit action potentials (MUPs) at maximum bladder filling was significantly larger than that at rest in the normal volunteers, patients with outlet obstruction, and sphincter dyssynergia. In patients with PNI, MUPs were not increased. The MUP amplitude did not differ significantly among groups during bladder filling. In PNI group, MUP duration at rest tended to be larger than those in other groups. Firing rates at first desire to void and at maximum desire to void were significantly increased than that at rest in every groups except the PNI group. Effect of alpha-1 adrenergic blocking agent, phentolamine (5 mg intravenously), was examined on 3 patients with benign prostatic hypertrophy (BPH), and in 4 patients with sphincter dyssynertia. Effect of an alpha-1 adrenergic stimulating agent, norepinephrine (5 microgram/min intravenously), was also evaluated on 5 patients with PNI during bladder filling. Immediately after administration of phentolamine, number of MUPs was decreased in BPH and sphincter dyssynertia groups. But in 2 paraplegic patients having reflex bladder with sphincter dyssynergia, number of MUPs did not decrease. Even with the continuous intravenous administration of norepinephrine for the elevation of the blood pressure, number of MUPs did not increase in any PNI patients. Effect of intravenous administration of phentolamine to induce urethral pressure elevation and the recording of the evoked EMG from external urethral sphincter by electrical stimulation of the penile dorsal nerve was tested on 4 patients without PNI before and after the administration. Phentolamine lowered urethral pressure at membranous urethra, but no significant change of evoked urethral pressure response and EMG activities was observed. It is concluded that the decrease of MUP after phentolamine administration is due to the relaxation of periurethral part of external urethral sphincter, and clinical denervation supersensitivity of the external urethral sphincter after norepinephrine administration was not demonstrated in the PNI groups.