Neural control of internal anal sphincter function (original) (raw)
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Integrative control of rectoanal reflex in guinea pigs through lumbar colonic nerves
American journal of physiology. Gastrointestinal and liver physiology, 2002
The aim of the present study was to analyze the neuromodulation of rectoanal reflex activity by lumbar sympathetic nerves in guinea pigs. The mechanical activities of the rectum were recorded with a balloon connected to a pressure transducer, and those of the internal anal sphincter (IAS) were recorded with a custom-made strain gauge force transducer. Gradual and sustained rectal distension evoked the rectoanal reflex, causing cholinergic contractions of the rectum and synchronous nitrergic relaxations of the IAS. Section of the lumbar colonic nerves enhanced both rectal contractions and IAS relaxations. Section of the 13th thoracic cord abolished both rectal contractions and IAS relaxations, but section of the lumbar colonic nerves restored them. Lumbar sympathectomy and pithing sacral cords greatly diminished these rectal contractions and IAS relaxations, but the intrinsic reflex component remained. NG-nitro-L-arginine methyl ester enhanced the intrinsic reflex-mediated contractio...
Rectoanal inhibitory reflex following low stapled anterior resection of the rectum
Diseases of the Colon & Rectum, 1992
The rectoanal inhibitory reflex plays an important role in the normal mechanisms of anorectal continence. Anterior resection abolishes the reflex, but whether it recovers, particularly after inverted stapled anastomosis, is not clear. Anal manometry was performed on patients undergoing low anterior resection for carcinoma. Maximum anal resting pressure and the rectoanal inhibitory reflex were assessed preoperatively and up to two years postoperatively. The reflex was present in 43 of 46 patients (93 percent) preoperatively, in 8 of 45 patients (18 percent) on the 10th postoperative day, and in 6 of 29 patients (21 percent) between six months and one year following surgery. Twenty patients were studied more than two years postoperatively, and in 17 (85 percent) the reflex was demonstrated. In the majority of low anterior resection patients, the rectoanal inhibitory reflex is abolished by surgery, remains absent throughout the first year, and has recovered by the end of the second postoperative year. This may be important in the recovery of anorectal function in these patients. [Key words: Anal sphincter; Anal continence; Anterior resection] O'Riordain MG, Molloy RG, Gillen P, Horgan A, Kirwan WO. Rectoanal inhibitory reflex following low stapled anterior resection of the rectum. Dis Colon Rectum 1992;35:874-878.
Sympathetic and Parasympathetic Regulation of Rectal Motility in Rats
Journal of Gastrointestinal Surgery, 2009
Introduction The colon and rectum are regulated by the autonomic nervous system (ANS). Abnormalities of the ANS are associated with diseases of the colon and rectum while its modulation is a putative mechanism for sacral nerve stimulation. The purpose of this study is to establish a rat model elucidating the role of the efferent ANS on rectal motility. Materials and Methods Rectal motility following transection or stimulation of parasympathetic pelvic nerves (PN) or sympathetic hypogastric nerves (HGN) was measured with rectal strain gauge transducers and quantified as a motility index (MI). Colonic transit was measured 24 hours after transection by calculating the geometric center (GC) of distribution of 51 Cr Results and Discussion Transection of PN and HGN decreased MI to 518±185 g•s (p<0.05) and increased MI to 5,029± 1,954 g•s (p<0.05), respectively, compared to sham (975±243 g•s). Sectioning of PN and HGN decreased transit with GC= 4.9±0.2 (p<0.05) and increased transit with GC=8.1±0.7 (p<0.02), respectively, compared to sham (GC=5.8±0.3). Stimulation of PN and HGN increased MI to 831±157% (p<0.01) and decreased MI to 251±24% (p<0.05), respectively. Conclusion Rectal motility is significantly altered by sectioning or stimulating either HGN or PN. This model may be useful in studying how sacral nerve stimulation exerts its effects and provide insight into the maladies of colonic motility.
Temporary Sacral Nerve Stimulation Alters Rectal Sensory Function: A Physiological Study
Diseases of the Colon & Rectum, 2011
BACKGROUND: The indications for sacral nerve stimulation are increasing, but the mechanism remains poorly understood. OBJECTIVE: This study aimed to examine the effect of sacral nerve stimulation on rectal compliance and rectal sensory function. DESIGN: This was a prospective study. SETTINGS: This study took place at a university teaching hospital. PATIENTS: Twenty-three consecutive consenting patients (22 female; median age, 49 y) undergoing temporary sacral nerve stimulation for fecal incontinence were prospectively studied. Clinical response was assessed by the use of bowel diaries and Wexner scores. MAIN OUTCOME MEASURES: Anal manometry, rectal compliance, volume and pressure thresholds to rectal distension (barostat), and rectal Doppler mucosal blood flow were measured before and at the end of stimulation. RESULTS: Sixteen patients (70%) had a favorable clinical response. Median anal squeeze pressures increased with stimulation from 40 (range, 6-156) cmH 2 O to 64 (range, 16-243) cmH 2 O. Median rectal compliance did not significantly change with stimulation (prestimulation: 11.5 (range, 7.9-21.8) mL/mmHg, poststimulation: 12.4 (range, 6.2-22) mL/mmHg, P ϭ .941). Rectal wall pressures associated with urge (baseline: 15.4 (range, 11-26.7) mmHg, poststimulation: 19 (range, 11.1-42.7) mmHg, P ϭ .054) and maximal tolerated thresholds (baseline: 21.6 (8.5-31.9) mmHg, poststimulation: 27.1 (14.3-43.3) mmHg, P ϭ .023) significantly increased after stimulation. Rectal Doppler mucosal blood flow did not significantly change with stimulation (baseline: 125.8 (69.9-346.8), poststimulation: 112.4 (50.2-404.1), P ϭ .735). Changes in anal resting pressure and rectal wall pressures with stimulation were evident only in responders; however, changes in anal squeeze pressures were evident in both responders and nonresponders. LIMITATIONS: The study reports results following shortterm stimulation in a small but homogenous group of patients. A larger long-term study will follow. CONCLUSION: Temporary sacral nerve stimulation does not change rectal compliance, but is associated with significant changes to the pressure thresholds of rectal distension. This, together with the observation that outcome is not related to sphincter integrity, supports the hypothesis of an afferent-mediated mechanism of action.
Activation-dependent descending reflex evacuation motority of anal canal in rat model
Archives italiennes de biologie, 2010
The evacuative motor responses of the anal canal and recto-anal reflexes during defecation were studied in an isolated rat recto-anal model preparation using (i) partitioned organ bath, (ii) electrical stimulation, (iii) balloon distension and (iv) morphological techniques. Electrical field stimulation applied to the anal canal or to the distal part of the rectum elicited tetrodotoxin (10(-7) M)-sensitive frequency-dependent local or descending contractions of the anal canal and the local responses were bigger in amplitude (14.9 ± 1.35 mN) than the descending contractions (5.3 ± 0.7 mN at frequency of 5 Hz, p < 0.05). The balloon-induced distension of the distal rectum evoked descending responses of the anal canal consisting of a short contraction (1.50 ± 0.18 mN) followed by deep relaxation (3.12 ± 0.34 mN). In the presence of atropine (3 x 10(-7) M) the electrically-elicited (5 Hz) local or descending contractions of the anal canal were suppressed and a relaxation revealed. The...
AJP: Gastrointestinal and Liver Physiology, 2008
Moderate rectal distension elicits recto-rectal reflex contractions and simultaneous recto-internal anal sphincter reflex relaxations that together comprise the defecation reflex. Both reflexes are controlled by 1) pelvic nerves, 2) lumbar colonic nerves, and 3) enteric nervous system. The aim of the present study was to explore a novel approach to repairing the defecation reflex dysfunction by using the plasticity of enteric nervous pathways. Experiments were performed in anesthetized guinea pigs with ethyl carbamate. The rectum 30 mm oral from the anal verge was transected without damage to extrinsic nerves, and subsequent end-to-end one-layer anastomosis was performed. Recovery of the defecation reflex and associated reflex pathways were evaluated. Eight weeks after sectioning of intrinsic reflex nerve pathways in the rectum, the defecation reflex recovered to the control level, accompanied with regeneration of reflex pathways. The 5-HT4-receptor agonist mosapride (0.5 and 1.0 mg...
Localisation and preservation of the autonomic nerves in rectal cancer surgery - technical details
Chirurgia (Bucharest, Romania : 1990)
Iatrogenic surgical injury to pelvic autonomic nerves followed by genitourinary dysfunctions are well known problems after total partial mesorectal excision for rectal cancer. The purpose of our paper is to present the useful anatomical landmarks for a safe nerve-sparing surgery in rectal oncology. Over the course of a total mesorectal excision we describe and illustrate the key risk zones of autonomic nerve injury based on our experience in rectal surgery and on the revised literature.
Physiological and pharmacological studies of the internal anal sphincter in the rat
Journal of Pediatric Surgery, 1984
9 The rectoanal reflex in the rat consists of relaxation followed by contraction of the internal anal sphincter (IAS). Beta-adrenergic drugs produce prolonged relaxation of the IAS, where e-agonists cause brief relaxation followed by contraction, iuscarinic cholinergic drugs contract the IAS. ATP and related purines produce relaxation which is blocked by theophylline. The reflex persists during adregeneric, cholinergic, and purinergic block. The potassium-blocker apamin prevents the relaxation induced by rectal distension. This suggests that the reflex is not mediated by adrenergic, cholinergic, or purinergic transmitters. Blocking potassium conductance was apparently the only way to eliminate this reflex.
Neuromyogenic properties of the internal anal sphincter: therapeutic rationale for anal fissures
Gut, 2000
Lateral sphincterotomy diminishes internal anal sphincter hypertonia and thereby reduces anal canal pressure. This improves anal mucosal blood flow and promotes the healing of anal fissures. However, sphincterotomy can be associated with long term disturbances of sphincter function. The optimal treatment for an anal fissure is to induce a temporary reduction of anal canal resting pressure to allow healing of the fissure without permanently disrupting normal sphincter function. Broader understanding of the intrinsic mechanisms controlling smooth muscle contraction has allowed pharmacological manipulation of anal sphincter tone. We performed an initial Medline literature search to identify all articles concerning "internal anal sphincter" and "anal fissures". This review is based on these articles and on additional publications obtained by manual cross referencing. Internal anal smooth muscle relaxation can be inhibited by stimulation of nonadrenergic non-cholinergic enteric neurones, parasympathetic muscarinic receptors, or sympathetic adrenoceptors, and by inhibition of calcium entry into the cell. Sphincter contraction depends on an increase in cytoplasmic calcium and is enhanced by sympathetic adrenergic stimulation. Currently, the most commonly used pharmacological agent in the treatment of anal fissures is topical glyceryl trinitrate, a nitric oxide donor. Alternative agents that exhibit a similar eVect via membrane Ca 2+ channels, muscarinic receptors, and or adrenoceptors are also likely to have a therapeutic potential in treating anal fissures.