Disposable Vaginal Surface Electrode for Urethral Sphincter Electromyography

Scandinavian Journal of Urology and Nephrology

Lose

Colstrup

et al. 1992

The influence of noradrenaline and prazosin on the urethral closure function was evaluated in 10 healthy female volunteers. Measurements of pressure at varying cross sectional areas were carried out at the bladder neck, in the high pressure zone, and in the distal urethra. Prazosin reduced the static pressure, predominantly in the midportion of the urethra, whereas noradrenaline caused no significant pressure change. The urethral resistance to dilatation and the hysteresis were unaffected by the two agents. It is suggested that the response to prazosin is related to decreased activity of the urethral smooth as well as of the striated muscles, the latter as a result of a reduced somatomotor output from the central nervous system.

Section: Methodsmentioning

confidence: 99%

The Effect of α-Adrenoceptor Stimulation and Blockade on the Static Urethral Sphincter Function in Healthy Females

Scandinavian Journal of Urology and Nephrology

Lose

Colstrup

et al. 1992

“…The E M G signal from the pelvic floor was measured by surface electrodes placed at the midportion of the anterior vaginal wall to exclude striated muscle contraction (24).…”

Section: Methodsmentioning

confidence: 99%

The Urethral Resistance to Rapid Dilatation: An Analysis of the Effect of Autonomic Receptor Stimulation and Blockade and of Pudendal Nerve Blockade in Healthy Females

Scandinavian Journal of Urology and Nephrology

Lose

Colstrup

et al. 1995

The urethral closure function is based upon permanently as well as adjunctively acting closure forces during rest and stress episodes, respectively. During urine ingression intra- and peri-urethral structures are suddenly stretched resulting in a pressure response which strengthens the closure function by sustaining the resistance to dilatation of the urethra. A method for measurement of the resistance to rapid urethral dilatation was used to evaluate the influence of noradrenaline, prazosin, terbutaline, propranolol, carbachol, and atropine, as well as bilateral pudendal nerve blockades in 40 healthy women. The drugs caused no significant change in the urethral resistance to dilatation, whereas the pudendal blockade produced a significant (p < 0.05) reduction at the bladder neck and in the high pressure zone. Although a quantitative assessment of their contribution cannot be obtained from this study, it may be concluded that the striated muscles innervated by the pudendal nerve are of major importance for the urethral resistance to dilatation.

“…The time interval between the dilatations was at least 3 s, in order to avoid the influence of preconditioning. EMG signals from the pelvic floor were measured by surface electrodes placed at the midportion of the anterior vaginal wall to exclude striated muscle contraction during the measurements [80]. The CA, the pressures in the bladder and the cylinder, and the EMG signal were registered, processed and displayed on a sixchannel recording system (DISA URO-system 2100).…”

Section: Methodsmentioning

confidence: 99%

An analysis of urethral viscoelasticity with particular reference to the sphincter function in healthy women

1995

Int Urogynecol J

Urine ingression into the urethra involves stretching of the fibers, resulting in a pressure increase. This study describes the pressure response following a rapid urethral dilatation. A probe for simultaneous recording of cross-sectional area (dilatation) and pressure was used. The urethral dilatations were induced by a gravitationally operated pump. Fifteen healthy women were studied. The pressure response (viscoelastic reaction) is a steep increase with the maximum at the end of dilatation. The maximum pressure is followed by a pressure decay (stress relaxation) over the next few seconds. The pressure response was highly dependent on the size and rate of dilatation but not on the urethral site of measurement. The median pressure response to a dilatation of 10 mm 2 at a rate of 150 mm2/s (chosen arbitrarily within the physiological range) is 45 cmH20. The pressure response may account for 25% of the urethral resistance to dilatation.