Assessment of the reliability of cerebral potentials evoked by electrical stimulation of the anal canal

1997 ◽  
Vol 12 (6) ◽  
pp. 335-339 ◽  
Author(s):  
A. M. Leroi ◽  
P. Ducrotté ◽  
M. Bouaniche ◽  
J. Y. Touchais ◽  
J. Weber ◽  
...  
Author(s):  
Samuel Sorkhi ◽  
Youngjin Seo ◽  
Valmik Bhargava ◽  
Mahadevan Raj Rajasekaran

External anal sphincter (EAS), external urethral sphincters and puborectalis muscle (PRM) have important roles in the genesis of anal and urethral closure pressures. In the present study, we defined the contribution of these muscles alone and in combination to the sphincter closure function using a rabbit model and a high-definition manometry (HDM) system. A total of 12 female rabbits were anesthetized and prepared to measure anal, urethral, and vaginal canal pressures using a HDM system. Pressure was recorded at rest, and during electrical stimulation of the EAS and PRM. A few rabbits (n=6) were subjected to EAS injury and the impact of EAS injury on the closure pressure profile was also evaluated. Anal, urethral, and vaginal canal pressures recorded at rest and during electrical stimulation of EAS and PRM demonstrated distinct pressure profiles. EAS stimulation induced anal canal pressure increase whereas PRM stimulation increased the pressures in all the three orifices. Electrical stimulation of EAS after injury resulted in about 19% decrease in anal canal pressure. Simultaneous electrical stimulation of EAS and PRM resulted in an insignificant increase of individual anal canal pressures when compared to pressures recorded after EAS or PRM stimulations alone. Our data confirm that HDM is a viable system to measure dynamic pressure changes within the three orifices and to define the role of each muscle in the development of closure pressures within these orifices in preclinical studies.


1993 ◽  
Vol 36 (1) ◽  
pp. 55-60 ◽  
Author(s):  
P. Delechenault ◽  
A. M. Leroi ◽  
T. Bruna ◽  
P. Denis ◽  
J. Weber

1962 ◽  
Vol 39 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Roger A. Gorski ◽  
Charles A. Barraclough

ABSTRACT We have previously suggested that the failure of the androgen-sterilized, persistent-oestrous rat to ovulate, following electrical stimulation of the median eminence structures of the hypothalamus, is due to an insufficiency in adenohypophyseal LH concentration. Using the ovarian ascorbic acid technique for quantitative determination of pituitary LH content, the present studies have demonstrated that the sterile rat pituitary gland contains one-third the LH content of the normal prooestrous gland. Furthermore, not only does progesterone priming of this persistent-oestrous rat result in a 75 % increase in LH concentration, but on hypothalamic stimulation sufficient LH is released to induce ovulation. The decrease in LH concentration which accompanies ovulation in the progesterone-primed, sterile rat is approximately 45 % of the total gland content as compared with a 51 % decrease in pituitary content in the normal cyclic rat.


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