A study of the effect of distension of the rectosigmoid junction on the rectum and anal canal with evidence of a rectosigmoid-rectal reflex

PURPOSE: To elucidate the role of the rectosigmoid junction (RSJ) in the mechanism of defecation. METHOD: Fourteen healthy volunteers were enrolled in the study (10 men, 4 women; mean age 38.2 +/- 10.6 years). The pressures in the rectum, anal canal, and RSJ as well as rectal balloon expulsion were recorded in response to balloon distension of the RSJ in increments of 10 ml of carbon dioxide (CO2) to 50 ml. The experiments were repeated after individual anesthetization of the RSJ, rectum, and anal canal. The expulsion of a 50-ml distended balloon located in the anesthetized rectum was tested. RESULTS: RSJ distension with 10 ml of CO2 produced no significant pressure changes in the RSJ, rectum, or anal canal. A 20-ml distension effected a significant pressure rise in the RSJ (P < 0.05) and the rectum (P < 0.01) and a decline in the anal canal (P < 0.05); the rectal balloon was expelled to the exterior. Similar pressure changes (P > 0.05) were recorded with a 30-, 40-, and 50-ml balloon distension. The mean latency for the RSJ response was 12.6 +/- 2.2 ms and for the rectum 15.8 +/- 2.6 ms. The balloon, distended with 50 ml of CO2 and located in the rectum, was not expelled to the exterior. Balloon expulsion occurred only with distension with volumes of above 80 ml. Individual anesthetization of the RSJ, rectum, and anal canal followed by RSJ distension produced no significant pressure changes in RSJ, rectum, and anal canal as well as no rectal balloon expulsion. CONCLUSION: The rectal contraction upon RSJ distension affirms the hypothesis of the possible involvement of a reflex, which we term "rectosigmoid-rectal reflex." This reflex relationship is evidenced by reproducibility and its absence on anesthetization of either the RSJ or the rectum, both presumably representing the two arms of the reflex arc. It is postulated that stools passing from the sigmoid colon to the rectum distend the RSJ and evoke the rectosigmoid-rectal reflex, which produces rectal contraction. The role of the reflex in defecation disorders needs to be studied.     

Effect of sigmoid colon distension on the rectosigmoid junction. Description of the rectosigmoid junction tightening reflex and its clinical implications

PURPOSE: The sigmoid colon (SC) is the site of stool storage. The stools accumulate in the SC until, at a certain volume, the mechanoreceptors in the SC wall are stimulated, evoking the sigmoidorectal junction inhibitory reflex with a resulting SC contraction, rectosigmoid junction (RSJ) relaxation and passage of the stools to the rectum. However, the RSJ status during stool accumulation in the SC has been scarcely addressed in the literature. The current study investigated this point. METHODS: A balloon-ended tube was introduced into the SC of 21 healthy volunteers [mean age (+/- SD) 36.8 +/- 10.3 years; 15 men and 6 women]. The pressures in the SC and RSJ were measured by means of a perfused tube, at rest and during balloon inflation with carbon dioxide at two rates: slow (3 ml/min) and rapid (150 ml/min). The tests were repeated after individual anesthetization of the SC and RSJ. RESULTS: During slow SC distension up to 80 ml included, the RSJ pressure progressively increased while the SC exhibited no pressure response (p > 0.05). At a distending volume of 100 ml, the pressure in the SC rose (p < 0. 01) and declined in the RSJ (p < 0.05), and the balloon was dispelled to the rectum. Rapid SC distension up to 40 ml included, effected no SC pressure response (p > 0.05) while the RSJ showed progressive pressure elevation. At 60 ml distension, the SC recorded a pressure rise (p < 0.001) and the RSJ a pressure decrease (p < 0. 05); the balloon was dispelled to the rectum. The pressure in the RSJ did not respond to distension of the anesthetized SC. CONCLUSION: The study has shown that, during accumulation of stools in the SC, leakage to the rectum seems to be prevented by a reflex action which we call 'rectosigmoid junction tightening reflex'. This reflex probably acts to control both storage and emptying of the SC contents. Reflex dysfunction might lead to defecation disorders. We suggest that the RSJ tightening reflex be included as an investigative tool in the diagnosis of defecation disorders.     

Study of the effect of colonic mass movements on the rectosigmoid junction with evidence of colo-rectosigmoid junction reflex.

Mass movements of the left-sided colon bring the colonic material contained in it to the sigmoid colon. The cause why the colonic contents do not pass directly to the rectum but stop short of the rectosigmoid junction (RSJ) was studied. The study comprised 10 healthy volunteers (mean age 39.2 +/- 10.2 years; 8 men, 2 women). A condomended tube was introduced into the descending colon (DC) per anum. The pressure response of the DC, sigmoid colon (SC), and RSJ to condom inflation with carbon dioxide (CO2) in increments of 10 ml was recorded by means of a three-channel microtip catheter. The responses were registered upon inflation of the upper, middle, and lower third of the DC. The test was repeated after individual anesthetization of the descending colon and the RSJ on separate days. Colonic distension with 10 and 20 ml CO2 produced no significant pressure changes in the DC, SC, and RSJ (p > .05); 30 ml distension effected a pressure rise in both the DC (p < .01) and RSJ (p < .05), but no change in the SC pressure (p > .05); and 40, 50, and 60 ml distension produced pressure changes similar to those obtained with 30 ml distension. The RSJ pressure responded to distension of the saline-injected but not of the anesthetized DC. Thus, the RSJ response to colonic distension affirms the hypothesis of the possible involvement of a reflex, which we term colo-RSJ reflex. This reflex seems to regulate the passage of stools from the colon to the rectum. Further studies are required to investigate its role in the diagnosis of defecation disorders.     

Effect of rectal distension on vesical motor activity in humans: the identification of the recto-vesicourethral reflex

OBJECTIVE: Rectal lesions have an effect on the urinary bladder and its sphincters. Patients with constipation sometimes complain of difficult micturition or of retention. Urinary retention may also occur after anorectal operations. We investigated the hypothesis that rectal distension affects vesical dilatation through a reflex action. METHODS: The study comprised 22 healthy volunteers (14 men, 8 women, age 42.3 +/- 10.3 SD years). The rectum was distended by rectal balloon inflated with air in increments of 50 mL. The vesical and posterior urethral pressures were recorded before and after individual anesthetization of the rectum, bladder, and posterior urethra. RESULTS: Fifty-milliliter rectal distension effected no vesicourethral pressure response (P > 0.05). At 100 and up to 300-mL distension, the vesical pressure decreased (P < 0.05), while the urethral pressure increased (P < 0.05). The response showed no significant difference upon increase of the distending volume. The mean latency was 16.8 +/- 2.4 milliseconds. Vesicourethral pressure did not respond to rectal distension when the bladder, urethra, or rectum was individually anesthetized. CONCLUSIONS: Rectal distension seems to induce diminished vesical, but increased urethral sphincter tone, an effect that is presumably mediated through a reflex that we call the "recto-vesicourethral reflex." This reflex is apparently evoked at defecation to abort simultaneous micturition. The clinical significance of the reflex needs to be established.     

Colosigmoid junction: a study of its functional activity with identification of a physiologic sphincter and involvement in reflex actions.

The colosigmoid junction (CSJ) marks the termination of the descending colon (DC) and the beginning of the sigmoid colon (SC); it is a fixed area in the retroperitoneum. At this site where two functionally different areas meet, we hypothesized the presence at the CSJ of a physiologic sphincter that regulates the passage of gut contents from the DC to the SC. This hypothesis was investigated for this communication. Eight subjects (mean age 36.6 +/- 4.7 SD years, 6 women) were studied during surgical repair of incisional hernia or laparotomy. The pressure responses of the CSJ to individual distension of the DC and SC were recorded. A balloon-ended tube was introduced per annum to lie in the DC or SC, and the pressure in the DC, CSJ, and SC was measured by saline-perfused catheters. To study whether the CSJ response to individual DC or SC distension was a direct or reflex action, the test was repeated in six of eight patients after separate anesthetization of the DC, CSJ, and SC. The CSJ had a higher pressure than that of the DC or SC; the high-pressure zone measured a mean of 2.1 +/- 0.9 cm. High-volume DC distension effected a significant DC pressure rise (p <.001) and a CSJ pressure decline (p <.05), which lasted a mean of 7.2 +/- 1.2 s. In contrast, the CSJ responded to big volume SC distension by significant pressure elevation (p <.001) which was also momentary. Small volume distension of the DC or SC effected no significant CSJ pressure response (p >.05). The CSJ pressure did not respond to distension of the anesthetized DC or SC. Likewise, the anesthetized CSJ did not react to DC or SC distension. When the test was repeated using saline instead of xylocaine, the CSJ pressure response was similar to that without saline injection. The CSJ is a high pressure zone with a measurable length. It reacts to DC or SC balloon distension by dilatation or narrowing, respectively. These findings presumably denote the existence of a "physiologic sphincter" at the CSJ, which appears to regulate the passage of colonic contents to the SC. We postulate that the CSJ pressure response to DC or SC distension is reflex and mediated through the "colosigmoid reflexes." The role of the colosigmoid sphincter and reflexes in colonic motility disorders remains to be investigated.     

Study of the role of the second defecation reflex: anorectal excitatory reflex in the pathogenesis of constipation

BACKGROUND: Previous studies have shown that anal distension caused rectal contraction, an action mediated through the anorectal excitatory reflex. Anal anesthetization aborted rectal contraction and rectal evacuation was induced by excessive straining. We investigated the hypothesis that inhibition or absence of the anorectal excitatory reflex could lead to constipation. METHODS: We studied 18 patients (mean age +/- SD: 40.6 +/- 5.8 years, 14 women) with rectal inertia, 14 (41.7 +/- 6.6 years, 12 women) with puborectalis paradoxical syndrome, and 10 healthy volunteers (37.9 +/- 4.8 years, 8 women). The rectum was filled with normal saline until urge and then evacuated; residual fluid was calculated. The anal and rectal pressure response to anal balloon distension in increments of 2 mL of saline was recorded by a two-channel microtip catheter. RESULTS: In the healthy volunteers, saline was evacuated as a continuous stream without straining except occasionally at the start of evacuation; no residual fluid was encountered. Anal balloon distension effected notable rectal pressure increase. In rectal inertia patients, evacuation occurred in small fluid gushes produced with excessive straining; residual fluid of large volume was collected. Anal balloon distension up to 10 mL produced no notable rectal pressure changes. The patients with PPS failed to evacuate more than a few mL of fluid despite excessive straining; the volume of residual fluid was considerable. Anal balloon distension caused a notable rectal pressure rise. The results were reproducible. CONCLUSIONS: These results suggest that the defecation reflexes (rectoanal and anorectal) are absent in rectal inertia patients and this presumably denotes a neurogenic disorder. The anorectal reflex is active in puborectalis paradoxical syndrome, but the rectoanal reflex is not, indicating a possible myogenic defect in the puborectalis muscle.     

Electromyographic activity of the anterolateral abdominal wall muscles during rectal filling and evacuation

BACKGROUND: The role of the anterolateral abdominal wall muscles (AAWMs) at defecation has not received sufficient attention in the literature. We investigated the hypothesis that the AAWMs exhibit increased electromyographic (EMG) activity on rectal distension, which presumably assists in rectal evacuation. MATERIALS AND METHODS: The effect of rectal balloon distension on the AAWMs EMG and on anal and rectal pressure was examined in 23 healthy volunteers (37.2 +/- 9.4 SD years, 14 men, 9 women); this effect was tested before and after rectal and AAWMs anesthetization. RESULTS: The rectal and anal pressures increased gradually upon incremental rectal balloon distension starting at 70 mL balloon distension until, at a mean of 113.6 +/- 5.6 mL, the balloon was expelled to the exterior. The AAWMs showed no EMG activity at rest or on rectal distension up to the time of balloon expulsion when they exhibited significant increase of EMG. This effect was abolished on individual rectal or AAWMs anesthetization but not with saline administration. CONCLUSIONS: AAWMs appear to contract simultaneously with rectal contraction; this action seems to increase the intra-abdominal pressure and assist rectal evacuation. The AAWMs contraction upon rectal contraction appears to be mediated through a reflex, which we call the "recto-abdominal wall reflex". Further studies are required to investigate the role of this reflex in defecation disorders.     

Effect of pelvic floor muscle contraction on vesical and rectal function with identification of puborectalis-rectovesical inhibitory reflex and levator-rectovesical excitatory reflex

 The effects of pelvic floor muscle contraction on rectal and vesical function were studied in 19 healthy volunteers with the aim of shedding light on some of the hitherto vague aspects of the mechanisms involved in micturition and defecation and their disorders. Rectal and vesical pressures were recorded during puborectalis (PR) and levator ani (LA) muscle stimulation with the rectum or urinary bladder empty and full. Muscle stimulation was effected by needle EMG electrode. The pressure responses to stimulation of the PR and LA muscles were also recorded with these muscles and the rectum and urinary bladder individually anesthetized in 12 of the 19 subjects. The test was repeated using saline instead of xylocaine. PR and LA muscle stimulation produced no pressure response in the empty rectum or bladder. Upon rectal balloon distension with a mean of 156.6 ± 34.2 ml of carbon dioxide the mean rectal pressure was 64.6 ± 18.7 cm H₂O, the subject felt the urge to evacuate and the balloon was expelled to the exterior. On PR muscle stimulation at rectal distension with the above volume, the subject did not feel the urge to evacuate, the rectal pressure was 8.2 ± 1.6 cm H₂O and the balloon was not expelled. Upon LA stimulation at the same volume, the urge persisted, the rectal pressure was higher and the balloon was expelled. Vesical filling with a mean of 378.2 ± 23.6 ml of saline initiated the urge to urinate and elevated the vesical pressure. PR muscle stimulation at this volume aborted the urge and pressure elevation, while LA stimulation caused more elevation of the vesical pressure and spontaneous micturition. Bladder filling with a mean of 423.6 ± 38.2 ml produced high vesical pressure and spontaneous urination, both of which were prevented by PR muscle stimulation but not by LA muscle stimulation. Stimulation of the PR and LA muscles during individual anesthetization of the rectum, bladder or PR and LA muscles resulted in no significant rectal or vesical pressure changes. Repetition of the test using saline instead of xylocaine resulted in rectal and vesical pressure responses similar to those without the use of saline. In conclusion, the decline in rectal and vesical responses upon PR muscle contraction indicates a reflex relationship which we term `puborectalis rectovesical inhibitory reflex'. This reflex is suggested to abort the urge to defecate or urinate. In contrast, LA muscle contraction produced rectal and vesical pressure elevation which is suggested to be mediated through the `levator rectovesical excitatory reflex'. `This reflex is probably evoked to promote rectal and vesical evacuation.     

Parasympathetic extrinsic reflex: role in defecation mechanism

The rectum has an intrinsic nervous mechanism represented by the enteric nervous plexus (ENP) and an extrinsic one mediated by the parasympathetic nerves. Rectal distension evokes the rectoanal inhibitory reflex, which acts through the ENP and is considered the main mechanism responsible for defecation. However, the role of the parasympathetic innervation compared to the role of the intrinsic mechanism of the defecation act has so far not been sufficiently addressed in the literature. The current study investigated this point. Twelve dogs were anesthetized. The anal and rectal pressures were recorded during rectal balloon distension with normal saline in 10 ml increments until the balloon was expelled to the exterior. The test was repeated after ENP block with a (phentolamine) and b (propranolol) adrenoceptor blocking agents and then after rectal denervation by bilateral pelvic ganglionectomy. The rectal balloon was expelled to the exterior at rectal balloon distension with 30 to 40 ml. After separate administration of phentolamine and propranolol, it was dispelled at a distending volume of 50 to 60 ml, and after rectal denervation at a volume of 80 to 90 ml. The results were reproducible. The balloon expulsion test suggests that the intrinsic defecation reflex is weaker than the extrinsic one for inducing defecation, although the two reflexes appear to be complementary. The difference between them in inducing defecation might be significant to our understanding the defecation act in the neurogenic rectum, a point that needs further study.     

Mechanism of ejection during ejaculation: identification of a urethrocavernosus reflex

The ejaculatory mechanism involves 2 reflexes: the "glans-vasal," which seems to bring the semen to the posterior urethra (emission phase of ejaculation), and the "urethromuscular" which ejects it to the exterior (ejection phase). This study investigated the mechanism of bulbocavernosus muscle (BCM) contraction, once the seminal fluid reaches the bulbous urethra. The study included 14 healthy male volunteers (mean age 37 +/- 10.2 SD years). To test the response of the BCM to urethral distension, a 10F balloon-tipped catheter was introduced into the prostatic urethra and filled with saline in increments of 0.25 mL: a needle electrode recorded the response. The balloon was then withdrawn to lie in the membranous. bulbous, and pendulous urethra and the test was repeated at each site. The latency of the muscle response was calculated. The BCM response to each of the anesthetized bulbous urethra and anesthetized BCM was recorded. Distension of the prostatic, membraneous, or pendulous urethra effected no BCM EMG response. Bulbous urethral distension with 0.25 mL of saline also produced no muscle response, whereas distension with 0.5 mL and up to 1.5 mL caused increased EMG activity of the BCM. The muscle response augmented with the increase of the distending volume. The mean latency was 10 +/- 1.3 ms and showed no significant change (p > .05) with the different distending volumes. Neither the anesthetized bulbous urethra nor the anesthetized BCM responded to bulbous urethral distension. The BCM contraction upon distension of the bulbous urethra is probably reflex and mediated through the urethrocavernosus reflex. Small-volume distension did not effect BCM contraction. The latter presumably propels the semen from the posterior to the pendulous urethra. It is suggested that the urethrocavernosus reflex be included in current andrologic investigations for patients with ejaculatory disorders.     

Effect of rectal distension on rectal electromechanical activity.

The rectum possesses electric activity in the form of pacesetter potentials (PPs) and action potentials (APs). The latter are associated with rectal pressure elevation and share in the rectal motile activity. A recent study has shown that electric waves are transmitted by the longitudinal but not the circular rectal muscle fibers. Rectal motile activity under normal physiologic conditions was suggested to be induced by the electric waves, that effect longitudinal muscle contraction, as well as by circular muscle stretch resulting from rectal distension. The current study investigated the effect of rectal overdistension on the rectal electromechanical activity aiming at assessing the effect of stool accumulation in the rectum on rectal motile activity. Under general anesthesia, the abdomen of 16 mongrel dogs was opened, the rectum exposed, and 3 electrodes were sutured to the rectal serosa. The rectal pressure was measured by a 10-F catheter connected to a pressure transducer. Rectal distension was achieved by a balloon inflated with carbon dioxide (CO2). Simultaneous recording of the electric activity and rectal pressure was performed during rectal inflation in increments of 10 mL CO2. There was significant increase of rectal pressure as well as of frequency, amplitude, and conduction velocity of PPs and APs on rectal distension. The more the rectal balloon was distended, the more was the increase in rectal pressure and waves variables; the increase was maximal just before balloon expulsion at 40 mL distension. Upon rectal overdistension (50 and 60 mL), no PPs or APs were recorded and the rectal pressure was 0; no balloon expulsion occurred. Rectal overdistension (pathologic distension) appears to abort the electromechanical activity of the rectum and lead to failure of the rectum to expel the balloon. This effect is suggested to be due to overstretch of rectal musculature with a resulting loss of the rectal electric waves and noncontraction of the muscle fibers. These findings appear to explain the cause of rectal atony, which occurs in rectal inertia and leads to constipation.     

The "opening time" and "pelvic floor electromyographic lag time": two novel tools in the assessment of the anorectal evacuation time.

Rectal evacuation necessitates rectal contraction and pelvic floor muscles relaxation; it is not known which action precedes the other. We investigated the hypothesis that pelvic floor muscles relaxation precedes rectal contraction so that rectal contents find the anal canal already opened. Electromyographic activity of the external anal sphincter as well as anal and rectal pressures were recorded during rectal balloon distension and evacuation. Pelvic floor muscles electromyographic lag time (time from start of pelvic floor muscles relaxation to start of evacuation) and opening time (time from start of rectal contraction to start of evacuation) were measured. Rectal balloon distension in increments of 20 mL up to 100 mL effected progressive increase of both external anal sphincter electromyography and anal pressure. At 120 mL balloon distension up to 180 mL, external anal sphincter electromyography and anal pressure exhibited gradual decrease whereas rectal pressure showed no changes. At 200 to 220 mL rectal balloon distension, rectal pressure increased and anal pressure decreased, while external anal sphincter showed no electromyographic activity; rectal balloon was expelled. The opening time recorded a mean of 1.8 +/- 0.7 s and pelvic floor muscles electromyographic lag time of 2.2 +/- 0.9; the two recordings showed no significant difference (p > .05). These, two diagnostic tools in anorectal investigations are presented: the opening time and pelvic floor muscles electromyographic lag time. Pelvic floor muscles relaxation preceded rectal contraction. As there is no significant difference between opening time and pelvic floor muscles electromyographic lag time, it appears easier to apply the latter as it is simple, objective, and noninvasive.     

Physiologic basis of digital-rectal stimulation for bowel evacuation in patients with spinal cord injury: identification of an anorectal excitatory reflex

BACKGROUND AND PURPOSE: Although advances in rehabilitation practices, pharmacology, and surgery offer new bowel program alternatives, digital-rectal stimulation is still utilized to facilitate defecation in patients with spinal cord injury (SCI). We speculated that defecation induced by such a technique is mediated through a reflex mechanism. METHODS: The study comprised 18 healthy volunteers (10 men, 8 women, mean age 36.6 +/- 9.7 years) and 9 patients with SCI (6 men, 3 women, mean age 35.1 +/- 11.2 years). The anal canal was dilated by a balloon inflated in 2-mL increments to 10 mL, and rectal pressure response was then recorded. The test was repeated after separate block of the external and internal anal sphincters and after individual anesthetization of the anal canal and rectum. RESULTS: In normal subjects, the rectal pressure rose significantly (p < 0.01) with 2-mL inflation. Increases in anal dilatation effected further rectal pressure elevations (p < 0.001), although there were no significant differences among the 4-, 6-, and 10-mL distensions (p > 0.05). The rectal pressure rise occurred with external, but not with internal, sphincter paralysis. In the subjects with paraplegia, there was no rectal pressure response to the 2- and 4-mL anal dilatations, while the 6-, 8-, and 10-mL distensions effected significant pressure increases (p < 0.001, p < 0.001, p < 0.001, respectively) that did not differ significantly among the 3 distending volumes. Internal sphincter inhibition, in contrast to the external sphincter, produced no rectal pressure response. In both normal subjects and subjects with paraplegia, the rectal pressure response did not occur after individual anesthetization of the rectum and anal canal. CONCLUSIONS: Anal dilatation induces rectal contraction through stimulation of mechanoreceptors, possibly in the internal sphincter. Rectal contraction upon anal dilatation suggests a reflex relationship that was absent on individual anesthetization of the possible 2 arms of the reflex arc: anal canal and rectum. This relationship, which we term the "anorectal excitatory reflex," appears to be evoked on digital anal dilatation. The reflex might be of diagnostic significance in defecation disorders and has the potential to be used as an investigative tool.     

Ureterovesical junction inhibitory reflex and vesicoureteral junction excitatory reflex: description of two reflexes and their role in the ureteric antireflux mechanism

The purpose of this study was to investigate the response of the ureterovesical junction (UVJ) to ureteric distension and to bladder filling with the aim of elucidating the mechanism of UVJ antireflux. The study was performed on 13 healthy volunteers [age 41.4±10.2 (SD) years; nine men, four women]. A ureteric catheter connected to a pressure transducer was introduced into the ureter proper. After recording the ureteric pressure, the catheter was withdrawn to the bladder, and the resting pressures in the UVJ and bladder were registered. The catheter was positioned in the UVJ and a 3F balloon-tipped ureteric catheter was introduced into the ureter proper and filled with saline in increments of 1 ml. The pressure response of the ureter and UVJ to ureteric distension was recorded. The bladder was then filled with 400 ml saline at two rates, slow (10 ml/min) and rapid (150 ml/min), and UVJ pressure response was registered. The aforementioned tests were repeated after anesthetizing the UVJ, the bladder musculature surrounding the UVJ and the ureteric wall at the site of the ureteric distension, respectively. Ureteric distension of the lower 2–3 cm effected ureteric pressure elevation (P<0.05) and a UVJ pressure drop (P<0.05); no pressure response of the UVJ occurred upon ureteric distension above this level. Slow bladder filling induced an increase in the UVJ (P<0.01) and vesical (P<0.01) pressures only when vesical filling reached a mean of 219.6±79.4 ml and above. Upon rapid vesical filling, the pressure response occurred at a smaller volume (136.6±52.3 ml). The pressure response did not occur when the UVJ was anesthetized. The study showed that lower ureteric distension was associated with a UVJ pressure drop. This reflex relationship, which we call the “ureterovesical junction inhibitory reflex,” was reproducible and disappeared on anesthetizing the UVJ or ureter. Vesical filling above a certain volume induced a UVJ pressure increase which was reproducible and disappeared on anesthetizing the UVJ; we call this reflex relationship the “vesicoureteral junction excitatory reflex.” These two reflexes seem to regulate the entry of urine from the ureters to the bladder and prevent ureteric reflux during bladder filling. In conclusion, two reflexes are identified that might contribute to the mechanism of UVJ antireflux.     

Rectal pacing: pacing parameters required for rectal evacuation of normal and constipated subjects

BACKGROUND AND PURPOSE: Our previous studies have demonstrated that rectal electric waves start at the rectosigmoid junction (RSJ) and spread caudad along the rectum. A rectosigmoid pacemaker was postulated to exist at the RSJ. We also demonstrated that electric waves in rectal inertia are so scarce that a "silent" electrorectogram is recorded; the myoelectric activity in such cases was stimulated by an artificial pacemaker placed at the RSJ. For this article we investigated the pacing parameters necessary for rectal evacuation in rectal inertia patients. METHODS: The study comprised 24 patients with rectal inertia divided into two groups: study group (10 women, 6 men; mean age, 38.9 +/- 10.6 years) and control group (6 women, 2 men; mean age, 36.3 +/- 9.8 years). The main complaint was infrequent defecation and straining at stools. Eight healthy volunteers (6 women, 2 men; mean age, 37.2 +/- 9.4 years) with normal stool frequency were included in the study. Through a sigmoidoscope, an electrode was hooked to the RSJ (stimulating) and two electrodes were hooked to the rectal mucosa (recording). Rectal electric activity was recorded before (basal activity) and during electric stimulation of the RSJ electrode with an electrical stimulator delivering constant electric current of 5-mA amplitude and 200-ms pulse width. RESULTS: In the healthy volunteers, rectal pacing effected increases in frequency, amplitude, and velocity from a mean of 2.3 +/- 0.9 to 6.2 +/- 1.8 cycles/min (P < 0.01), 1.2 +/- 0.6 to 1.7 +/- 0.8 mV (P < 0.05), and 4.1 +/- 1. 2 to 6.3 +/- 1.7 cm/s (P < 0.05), respectively. No waves were recorded from rectal inertia patients at rest. Rectal pacing of the study group showed pacesetter potentials with a mean frequency of 2. 1 +/- 1.2 cycles/min, amplitude of 0.9 +/- 0.1 mV, and velocity of 3. 3 +/- 1.6 ms. The control group, in whom the pacemaker was not activated, showed no electric activity. CONCLUSIONS: Rectal pacing succeeded in producing myoelectric activity in patients with rectal inertia. It is therefore suggested that this method be applied for rectal evacuation in patients with inertia constipation.     

The "uninhibited rectum": a cause of fecal incontinence

OBJECTIVE: The uninhibited (unstable) rectum has been defined as a cause offecal incontinence (FI) in patients with supraconal lesions. In this study, we tested the hypothesis that the uninhibited rectum may be a cause of FI in patients with normal anal pressure and sphincteric mechanism who were considered to have idiopathic FI. METHODS: The study comprised 82 patients (mean age 38.2 +/- 11.2 years; 58 women and 24 men) with idiopathic FI and a control group of 20 healthy volunteers (mean age 36.3 +/- 10.6 years; 14 women and 6 men). Inclusion criteria for FI patients were normal electromyogram of the external anal sphincter and puborectalis muscle, and normal anal sensation, pressure, and endosonography. Rectometry was performed using rectal balloon inflation with CO2 at a rate of 150 cc/min. Rectometrograms were assessed quantitatively and qualitatively. RESULTS: In 79 FI patients, the first rectal sensation was not felt. Urge was perceived at the time of balloon expulsion, which could not be prevented by voluntary sphincteric squeeze. In the remaining 3 patients, the first sensation was perceived but urge coincided with balloon expulsion. Rectometrography showed moderate and gross fluctuations in the tone limb that were not associated with significant changes in intra-abdominal pressure. This contrasted with normal subjects in whom the tone limb exhibited no fluctuations or minor fluctuations that roughly paralleled the intra-abdominal pressure fluctuations. The rectal distension volume at balloon expulsion was significantly lower in FI patients than in controls (P < .05). CONCLUSIONS: These findings suggest that FI can be explained by the fact that the first rectal sensation was that of urge, which was perceived synchronously with balloon expulsion. That is, the balloon had been expelled before the patient could voluntarily squeeze the sphincters to abort expulsion. We postulated that during inflation with small volumes, the rectum did not adapt as in controls, but responded with contractions, which appear to be reflected in the multiple fluctuations in the tone limb. FI in these patients appears to be a consequence of the unstable or uninhibited rectum.     

Role of the enteric nervous plexus in rectal motile activity: an experimental study.

The gut innervation is formed by an intrinsic and an extrinsic component. The former is responsible for the intestinal contractions that occur in the total absence of extrinsic innervation. We hypothesize that the intrinsic plexuses do not produce local contraction, but mediate reflex actions of the gut musculature. This hypothesis was investigated in the rectum of the experimental animal. In 16 anesthetized mongrel dogs, the rectum was exposed, and 3 monopolar silver-silver chloride electrodes were sutured serially to the rectal wall and connected to a rectilinear pen recorder. The rectal electric activity was recorded at rest and on rectal inflation while the anal pressure was synchronously registered. The tests were repeated after separate drug administration using phentolamine, propranolol (adrenoceptor blocking agents), atropine (cholinergic blocking agent), drotaverine (direct smooth muscle relaxant), and nitroglycerine. (NO donor, inhibitory noncholinergic, nonadrenergic mediator). Slow waves or pacesetter potentials (PPs) and action potentials (APs) were recorded from the three electrodes. Rectal balloon distension caused an increase of frequency, amplitude, and conduction velocity of these waves, as well as a decrease of anal pressure. Repetition of the test after administration of phentolamine, propranotol, and atropine effected no change in rectal electromyelographic (EMG) activity or anal pressure, while drotaverine and nitroglycerine administration aborted both the electric activity and the anal pressure response. We conclude that the rectal electric activity, presumably responsible for rectal motility, was not aborted by enteric nervous plexus block but by direct muscle relaxant. This suggests that the enteric plexus has no direct action on the rectal motile activity but mediates the rectal reflex actions. This concept might explain some of the hitherto unknown mechanisms of rectal dyssynergia syndromes.     

Preservation of continence after ileoanal anastomosis by the coordination of ileal pouch and anal canal motor activity.

Nocturnal incontinence may occur after ileoanal anastomosis and may be related to loss of an effective anal canal pressure barrier during sleep; how pressure and contractions in the proximal bowel influence this barrier is unknown. Our aim was to evaluate the relationship between anal canal pressure and contractions and contractile activity of the pouch in continent subjects after ileal pouch-anal anastomosis (IPAA) and of the rectum in normal controls. A fully ambulatory system for 24-hour pressure recording was used. A flexible transducer catheter was introduced endoscopically so that sensors were at 2, 3, 8, 12, 16, and 24 cm from the anal orifice in 12 healthy controls (7 men, 5 women, mean age: 35 years) and 7 fully continent IPAA patients (4 men, 3 women, mean age: 34 years) more than 12 months postoperatively. Twenty-four hour spontaneous motor activity was stored in a 2.5 megabyte (MB) digital portable recorder. Mean anal canal pressure was calculated, and rectal motor complexes and ileal pouch large pressure waves were characterized. During sleep, resting anal canal pressures were similar in the two groups (72 +/- 12 mm Hg in controls versus 66 +/- 9 mm Hg in IPAA patients [mean +/- standard deviation (SD)], p = NS), but anal canal pressure showed cyclic relaxations (periodicity: 95 +/- 11 min in controls, 54 +/- 18 min in IPAA patients, p less than 0.05), during which the mean pressure trough was 15 +/- 4 mm Hg in controls and 14 +/- 5 mm Hg in IPAA patients (p = NS). In the control patients, during sleep, a mean of six rectal motor complexes were identified (range: 3 to 9). In patients with IPAA, during sleep, a mean of eight large pressure waves per hour were identified (range: 2 to 20). Importantly, in both controls and patients, rectal motor complexes or large pressure waves were always accompanied by rapid return of anal canal pressure from trough to basal values and increased contractile activity. We concluded that, in healthy patients and in continent patients after IPAA, motor activity of the rectum and of the ileal pouch was associated with changes in pressure and contractile activity of the anal canal so that rectal- and neorectal-anal canal pressure gradient, and, in turn, fecal continence were preserved.     

Role of the Enteric Nervous Plexus in Rectal Motile Activity: An Experimental Study

The gut innervation is formed by an intrinsic and an extrinsic component. The former is responsible for the intestinal contractions that occur in the total absence of extrinsic innervation. We hypothesize that the intrinsic plexuses do not produce local contraction, but mediate reflex actions of the gut musculature. This hypothesis was investigated in the rectum of the experimental animal. In 16 anesthetized mongrel dogs, the rectum was exposed, and 3 monopolar silver-silver chloride electrodes were sutured serially to the rectal wall and connected to a rectilinear pen recorder. The rectal electric activity was recorded at rest and on rectal inflation while the anal pressure was synchronously registered. The tests were repeated after separate drug administration using phentolamine, propranolol (adrenoceptor blocking agents), atropine (cholinergic blocking agent), drotaverine (direct smooth muscle relaxant), and nitroglycerine. (NO donor, inhibitory noncholinergic, nonadrenergic mediator). Slow waves or pacesetter potentials (PPs) and action potentials (APs) were recorded from the three electrodes. Rectal balloon distension caused an increase of frequency, amplitude, and conduction velocity of these waves, as well as a decrease of anal pressure. Repetition of the test after administration of phentolamine, propranotol, and atropine effected no change in rectal electromyelographic (EMG) activity or anal pressure, while drotaverine and nitroglycerine administration aborted both the electric activity and the anal pressure response. We conclude that the rectal electric activity, presumably responsible for rectal motility, was not aborted by enteric nervous plexus block but by direct muscle relaxant. This suggests that the enteric plexus has no direct action on the rectal motile activity but mediates the rectal reflex actions. This concept might explain some of the hitherto unknown mechanisms of rectal dyssynergia syndromes.     

Pelviureteral inhibitory reflex and ureteropelvic excitatory reflex: Role of the two reflexes in regulation of urine flow from the renal pelvis to the ureter

The mechanism by which the ureteropelvic junction (UPJ) regulates the passage of urine from the renal pelvis to the ureter, and prevents urinary backflow from the ureter to the renal pelvis, is not completely understood. The current communication studies this mechanism in 18 dogs. With the dogs under anesthesia, nephrostomy was done through which two catheters (one pressure and one balloon-tipped) were introduced into the UPJ and the renal pelvis, respectively. Renal pelvis distension with a balloon filled with 1 ml of saline effected a rise of renal pelvic pressure from a mean basal pressure of 4.8 ± 1.2 cm H₂O to 6.9 ± 2.3 cm H₂O (P < 0.05). The basal UPJ pressure of 12.6 ± 2.7 cm H₂O showed no significant change with 1 ml distention of the renal pelvic balloon (P > 0.05). Renal pelvic distension with 2, 3, and 4 ml caused a significant rise of renal pelvic pressure to 8.4 ± 2.7 (P < 0.05), 10.6 ± 2.2 (P < 0.01), and 11.8 ± 1.9 (P < 0.01) cm H₂O, respectively, and a significant drop of UPJ pressure to 4.8 ± 1.2, 4.7 ± 1.1, and 4.6 ± 1.2 cm H₂O (P < 0.01), respectively. Ureteric distension with a balloon filled with 0.5 ml of saline significantly raised the ureteric pressure from a mean basal value of 4.3 ± 1.4 cm H₂O to 14.7 ± 3.3 cm H₂O (P < 0.01) and the UPJ pressure to a mean of 20.8 ± 3.8 (P < 0.05). Ureteric distension with 1 and 1.5 ml of saline led to an elevation of ureteric and UPJ pressure which was not significantly different from that observed with distension with 0.5 ml (P > 0.05). In contrast, the UPJ showed no significant pressure change upon distension of the locally anesthetized renal pelvis or ureter, respectively. Likewise, the locally anesthetized UPJ exhibited no significant pressure response to renal pelvic or ureteric distension. The study demonstrates that urine might have to accumulate in the renal pelvis up to a certain volume and pressure so as to effect UPJ opening, which occurs at its maximum irrespective of the distending volume. UPJ opening upon renal pelvic distension postulates a reflex relationship which we call “pelviureteral inhibitory reflex.” This reflex is believed to regulate the passage of urine from the renal pelvis to the ureter. Ureteric distension closes the UPJ we call this reflex action the “ureteropelvic excitatory reflex” as it seems to prevent reflux of urine through the UPJ and thus protects the kidney. The concept that the UPJ acts as a physiologic sphincter is put forward. Neurourol. Urodynam. 16:315–325, 1997. © 1997 Wiley-Liss, Inc.