Placement of a fine‐bore rectal balloon catheter in the anal canal does not affect anal sphincter pressures: improving our understanding of physiological function with anal acoustic reflectometry

2020 ◽  
Vol 22 (11) ◽  
pp. 1626-1631
Author(s):  
N. A. Heywood ◽  
A. Sharma ◽  
E. S. Kiff ◽  
N. Klarskov ◽  
K. J. Telford
2008 ◽  
Vol 134 (4) ◽  
pp. A-278
Author(s):  
Mahadevan R. Rajasekaran ◽  
Yanfen Jiang ◽  
Amir Motamedi ◽  
Ravinder K. Mittal

Radiology ◽  
2003 ◽  
Vol 229 (1) ◽  
pp. 99-108 ◽  
Author(s):  
Stuart A. Taylor ◽  
Steve Halligan ◽  
Vicky Goh ◽  
Simon Morley ◽  
Paul Bassett ◽  
...  

2015 ◽  
Vol 13 (10) ◽  
pp. 1793-1800.e1 ◽  
Author(s):  
David Prichard ◽  
Doris M. Harvey ◽  
Joel G. Fletcher ◽  
Alan R. Zinsmeister ◽  
Adil E. Bharucha

1988 ◽  
Vol 255 (3) ◽  
pp. G389-G394 ◽  
Author(s):  
S. Rattan ◽  
R. Shah

Studies were performed in alpha-chloralose-anesthetized and pancuronium-treated opossums. Resting internal anal sphincter pressures (IASP) were monitored using low-compliant continuously perfused catheters. P1 and P2 purinoceptor agonists, adenosine and ATP, respectively, administered close intra-arterially, caused dose-dependent decreases in the IASP. The inhibitory effect of these agonists on the IASP was tetrodotoxin resistant. Rectal balloon distension (RD) (which mimics the rectoanal inhibitory reflex) caused volume-dependent IAS relaxation. Electrical stimulation of the sacral nerve (SNS) also produced frequency-dependent decreases in IASP. The inhibitory response to adenosine (P1 purinoceptor agonist), ATP (P2 purinoceptor agonist), RD, and SNS on the internal anal sphincter (IAS) was examined before and after 8-phenyltheophylline (P1 purinoceptor antagonist) and alpha,beta-methylene ATP (P2 purinoceptor antagonist that irreversibly binds and desensitizes P2 purinoceptor). P1 and P2 purinoceptor antagonists produced selective antagonism of the inhibitory responses on the IAS of their respective agonists only. Furthermore, high doses of adenosine and ATP produced desensitization and block of their own actions only. The purinoceptors' antagonists, and the desensitization of purinoceptors by high doses of adenosine and ATP, failed to modify the fall in IASP in response to RD or SNS. From these studies we conclude that distinct inhibitory P1 and P2 purinoceptors are present on the IAS smooth muscle. However, these inhibitory purinoceptors may not be responsible for the rectoanal reflex-mediated IAS relaxation.


2010 ◽  
Vol 138 (5) ◽  
pp. S-541
Author(s):  
Mahadevan R. Rajasekaran ◽  
Yanfen Jiang ◽  
Amir Motamedi ◽  
Valmik Bhargava ◽  
Ravinder K. Mittal

2009 ◽  
Vol 52 (11) ◽  
pp. 1902-1911 ◽  
Author(s):  
Alvaro Opazo ◽  
Begoña Lecea ◽  
Carme Admella ◽  
Maria José Fantova ◽  
Marcel Jiménez ◽  
...  

Swiss Surgery ◽  
2003 ◽  
Vol 9 (4) ◽  
pp. 193-197 ◽  
Author(s):  
Gervaz ◽  
Hennig ◽  
Buechler ◽  
Soravia ◽  
Brigstock ◽  
...  

Background: There is accumulating evidence, both quantitative and qualitative, that pelvic irradiation affects anorectal function. However, the molecular mechanisms responsible for radiation-induced damage to the anal sphincter remain unclear. Aim: To determine the expression of transforming growth factor-beta1 (TGF-beta1) and its downstream effector connective tissue growth factor (CTGF) in the anal sphincter of a patient irradiated for prostate cancer. Patient: A 82 year-old patient developed a rectal adenocarcinoma and underwent an abdomino-perineal resection (APR), four years after receiving pelvic irradiation for prostate carcinoma. Methods: Tissue sections of the anal sphincter were processed for histology. Immunostaining for TGF-beta1 and CTGF were performed. Results: CTGF and TGF-beta1 immunoreactivity was detected in the irradiated anal sphincter, and was absent in controls. Immunoreactivity for both cytokines predominated in the internal sphincter. CTGF and TGF-beta1 were preferentially detected in endothelial cells, myofibroblasts and fibroblasts; in addition, there was strong immunoreactivity for TGF-beta1, but not for CTGF in smooth muscle cells of the anal canal. Conclusion: Four years after pelvic irradiation, radiation-induced damage appeared to affect predominantly the smooth muscle layer of the anal canal. The molecular mechanisms responsible for radiation-induced fibrosis to these tissues involve prolonged activation of TGF-beta1 and its downstream effector CTGF.


2011 ◽  
Vol 300 (2) ◽  
pp. G236-G240 ◽  
Author(s):  
Gregory Cheeney ◽  
Jose M. Remes-Troche ◽  
Ashok Attaluri ◽  
Satish S. C. Rao

Desire to defecate is associated with a unique anal contractile response, the sensorimotor response (SMR). However, the precise muscle(s) involved is not known. We aimed to examine the role of external and internal anal sphincter and the puborectalis muscle in the genesis of SMR. Anorectal 3-D pressure topography was performed in 10 healthy subjects during graded rectal balloon distention using a novel high-definition manometry system consisting of a probe with 256 pressure sensors arranged circumferentially. The anal pressure changes before, during, and after the onset of SMR were measured at every millimeter along the length of anal canal and in 3-D by dividing the anal canal into 4 × 2.1-mm grids. Pressures were assessed in the longitudinal and anterior-posterior axis. Anal ultrasound was performed to assess puborectalis morphology. 3-D topography demonstrated that rectal distention produced an SMR coinciding with desire to defecate and predominantly induced by contraction of puborectalis. Anal ultrasound showed that the puborectalis was located at mean distance of 3.5 cm from anal verge, which corresponded with peak pressure difference between the anterior and posterior vectors observed at 3.4 cm with 3-D topography ( r = 0.77). The highest absolute and percentage increases in pressure during SMR were seen in the superior-posterior portion of anal canal, reaffirming the role of puborectalis. The SMR anal pressure profile showed a peak pressure at 1.6 cm from anal verge in the anterior and posterior vectors and distinct increase in pressure only posteriorly at 3.2 cm corresponding to puborectalis. We concluded that SMR is primarily induced by the activation and contraction of the puborectalis muscle in response to a sensation of a desire to defecate.


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