Effect of renal pelvic distension on the ureteropelvic and ureterovesical junctions and the urinary bladder: the renal pelvivesical reflex

For investigation of the effect of distension of the renal pelvis on the ureteropelvic (UPJ) and uretero vesical junctions (UVJ) and on the urinary bladder, nephrostomy was performed on 14 anesthetized mongrel dogs. The pressure was measured in the UPJ by a catheter with a side port introduced through the nephrostomy and in the UVJ and urinary bladder by two catheters inserted cystoscopically. Likewise, a balloon mounted on the tip of a catheter was introduced into the renal pelvis. It was filled with saline in increments of 1 ml, and the pressure response of the UPJ, the UVJ, and the urinary bladder was determined. The test was repeated on the anesthetized renal pelvis, UVJ, and bladder. Whereas renal pelvic distension with 1 ml of saline effected no pressure response in the UPJ, UVJ or bladder, distension with 2–4 ml produced a significant pressure drop (P < 0.01, P < 0.01, and P < 0.05, respectively). There was no difference in the pressure drops recorded at distensions with 2, 3, or 4 ml of saline (P > 0.05). Distension of the anesthetized renal pelvis produced no pressure response in the UPJ, UVJ, or bladder. Furthermore, renal pelvic distension did not elicit a pressure response in the anesthetized UPJ or the bladder. In conclusion, the opening of the UVJ synchronously with the UPJ upon renal pelvic distension appears to assist the delivery of urine from the renal pelvis to the urinary bladder and to protect both the renal pelvis and the ureter against dilatation. This process is supported by a vesical pressure drop. The opening of the UPJ together with the UVJ and the vesical relaxation observed on renal pelvic distension seem to be reflex in nature. A “renal pelvivesical reflex” is postulated to regulate the flow of urine from the renal pelvis to the urinary bladder, preventing the occurrence of urine collection in, or backflow into, the renal pelvis or the ureter.     

Rectourethral reflex: description of a reflex and its clinical significance. A preliminary report.

The present communication studies the technique and clinical significance of a new reflex which I called 'rectourethral reflex'. The study comprised 29 subjects with normal anorectal and urinary functions. The procedure consisted of inflating the rectum with a balloon connected to the distal part of a catheter. The electromyographic activity of the external urethral sphincter was recorded using a concentric needle electrode inserted into the muscle. The procedure was repeated in 10 patients after muscle infiltration with Xylocaine or saline. Rectal distension evoked external urethral sphincter contraction in all the subjects. The amplitude of motor action potentials increased with increasing rectal distension. Anesthetized muscles did not respond, while saline-infiltrated muscles responded. The latency of the reflex decreased with increasing volume of rectal inflation. The reflex harmonizes the relation between defecation and micturition. It guards against involuntary micturition when the rectal detrusor is distended. Changes in amplitude and latency of the reflex may be significant in assessing rectourinary disorders. The reflex could thus be used as an investigative tool in the diagnosis of such disorders.     

Effect of magnetic stimulation on the contractile activity of the rectum in humans

Magnetic stimulation (MS) has been used to activate the neuromuscular tissue by inducing an electric field. Based on the results of a recent study on a canine model (Eur Surg Res 1998;30:268-72), which demonstrated that sacral MS effected a rectal and vesical pressure rise and a drop of rectal neck (anal canal) pressure, thereby achieving evacuation, the test was performed on 28 healthy volunteers (mean age, 36.6 years; 18 men and 10 women). The rectal, rectal neck, and vesical pressures were recorded during sacral MS with a magnetic coil while the rectum was empty and distended by a balloon. Electromyographic activity of the two rectus abdominis muscles was determined to exclude the possible interference of intra-abdominal pressure with the MS recordings. Stimulation parameters were set at 70 per cent intensity, 40-Hz frequency, and 1-to 2-second burst length. Sacral MS effected significant rectal and vesical pressure rise (P < 0.01 and P < 0.01, respectively) and drop of rectal neck pressure (P < 0.01). Intermittent stimulation induced balloon expulsion from the rectum. The two rectus abdominis muscles did not show change in electromyographic activity during MS, indicating that the rectal and vesical pressure rise was not due to increased intra-abdominal pressure. Sacral MS induced rectal evacuation with no adverse effects. The method is simple, easy, safe, and noninvasive and is suggested to be applied for the treatment of the inertic or neuropathic rectum. As the vesical pressure proved to be elevated too, MS might also be used for rectal and vesical evacuation in patients with spinal cord lesions.     

Effect of vesical contraction on the non-sphincteric part of the urethra: Recognition of vesicourethral inhibitory reflex

OBJECTIVES: The effect of vesical contraction on the non-sphincteric part of the urethra has been scarcely addressed in the literature. In this study, the hypothesis that detrusor contraction effects dilatation of the non-sphincteric part of the urethra was investigated. METHODS: Non-sphincteric urethral pressure response to vesical balloon distension with normal saline in increments of 50 mL was recorded in 21 healthy volunteers (mean age 40.7 +/- 10.3 years, 13 men) before and after individual anesthetization of the urethra and urinary bladder. Vesical distension was effected by a 10F balloon-ended catheter introduced into bladder per urethram. Urethral and vesical pressures were measured by means of a two-channel microtip catheter. RESULTS: Small-volume vesical distension effected no significant urethral or vesical pressure changes while distension with 350 and 400 mL of saline produced vesical pressure elevation (P < 0.01) and urethral pressure decrease (P < 0.01). Vesical distension after individual vesical and urethral anesthetization effected no change in the urethral pressure. These results were reproducible. CONCLUSIONS: Dilatation of the non-sphincteric part of the urethra upon vesical contraction is suggested to be mediated through a 'vesicourethral inhibitory reflex' and to facilitate passage of urine through the urethra. The reflex may prove to be of diagnostic significance in micturition 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.     

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.     

Baroreceptor-heart rate reflex sensitivity enhancement after urinary bladder distention in essential hypertensives

Our objective was to determine if urinary bladder distention modifies the sensitivity of the baroreceptor-heart rate reflex in hypertensive and control subjects. The baroreceptor-heart rate reflex sensitivity was measured in 15 male patients (mean age 37 ± 8 years) with mild untreated hypertension (mean 163 ± 8/95 ± 12 mmHg) and 17 age- and sex-matched control subjects before and after urinary bladder distention. Bladder filling was performed infusing saline heated to 37°C via a urinary catheter; the volume infused in each patient corresponded to that which caused the urge to void without reaching the pain threshold. The baroreceptor-heart rate reflex sensitivity was determined correlating the variations of the systolic pressure and of the peak blood flow velocity in the common carotid artery with the variations of the ECG RR′ interval of the following heart beat, both during spontaneous and phenylephrine-induced fluctuations of the haemodynamic variables. After bladder distention the diastolic pressure of the hypertensive subjects increased significantly (95 ± 12 vs. 100 ± 12 mmHg; P < 0.02), whereas the heart rate decreased (RR=873 ± 70 vs. 926 ± 80 ms; P < 0.005). These parameters were unchanged in the normotensive subjects (84 ± 9 vs. 83 ± 8 mmHg and 914 ± 158 vs. 913±140 ms, respectively). The baroreceptor-heart rate reflex sensitivity, measured on the basis of spontaneous pressure and carotid blood flow velocity fluctuations in relationship to RR changes, decreased in the normotensive subjects after bladder distention (10.7 ± 4.6 vs. 9.4 ± 2.7 ms/mmHg; P < 0.05 and 423 ± 99 vs. 356 ± 102 ms/kHz; P < 0.01, respectively), whereas it increased in the hypertensive patients (6.9 ± 3.6 vs. 8.3 ± 2.8 ms/mmHg; P < 0.03, and 332 ± 86 vs. 381 ± 97 ms/kHz; P < 0.03 respectively). After bladder distention and phenylephrine administration the baroreceptor-heart rate reflex sensitivity, measured by the correlation between systolic pressure and RR interval, increased only in the hypertensive group (10.2 ± 5.4 vs. 15.2 ± 7.7 ms/mmHg; P < 0.005). In conclusion urinary bladder distention provokes in hypertensives but not normotensive controls a brisk parasympathetic response of the component of the baroreceptor-heart rate reflex which controls heart rate. Received: 17 June 1998 / Accepted: 20 October 1998     

Findings of pelvic musculature and efficacy of laparoscopic muscle stimulator in laparoscopy-assisted anorectal pull-through for high imperforate anus

Background: Laparoscopic findings of levator muscle and the efficacy of laparoscopic muscle stimulator (LMS) in infants with high imperforate anus have not been reported. Methods: Twelve patients underwent laparoscopically assisted anorectoplasty for high imperforate anus. Following laparoscopic dissection of the distal rectum and division of the fistula, levator muscles in the pelvic floor were stimulated with a 5-mm-diameter LMS. Dilatation was done by inserting a guidewire and balloon catheter through the center of the levator muscle sling and muscle complex. Rectal pull-through and anastomosis between the rectum and anus were successfully completed. Results: LMS showed good contraction of levator muscles and enhanced accurate midline placement of pull-through rectum. LMS was particularly useful in observing weak muscles in infants with rectovesical fistula. Conclusions: Laparoscopy and LMS offer excellent visualization of the pelvic musculature and precise tract of rectal pull-through. Fecal continence will be assessed by long-term follow-up.     

Effect of renal pelvic and ureteral distension on the striated urethral sphincter with recognition of the “reno-vesico-sphincteric reflex”

Renal pelvic and ureteral distension occurs in physiologic (diuresis) and pathologic (calculus) conditions. Its effect on the vesical and posterior urethral pressures as well as on the electromyographic (EMG) activity of the striated urethral sphincter (SUS) was investigated. The renal pelvis of 10 healthy volunteers (7␣men, 3 women; mean age 35.8 ± 8.6 years) was distended by means of a 4-F balloon-tipped catheter in␣increments of 2 ml of saline up to 10 ml and the response of the vesical and posterior urethral pressures and SUS EMG activity was recorded. The test was repeated with ureteral distension in increments of 0.25 ml up to 1 ml. The response of the aforementioned parameters was also registered after anesthetization of the renal pelvis, ureter and SUS. Two rates of renal pelvic and ureteral distension were tested: rapid (1 ml/s) and slow (1 ml/min). Renal pelvic distension with large volumes effected an increase of the renal pelvic and urethral pressures (P < 0.05, P < 0.05, respectively), a vesical pressure drop (P < 0.05) and increased EMG activity of the SUS. Ureteral distension caused a rise of ureteral and urethral pressures as well as of SUS EMG activity. With rapid distension, the aforementioned parameters responded at smaller volumes than with slow distension. Renal pelvic, ureteral or SUS anesthetization effected no urethral or SUS EMG response. It is suggested that the reaction of above parameters to distension indicates a mechanism regulating the urine flow so as to protect the renal pelvis and the ureter from being overloaded. The vesical pressure drop with increased SUS EMG activity on renal pelvis distension postulates a reflex relationship that we call the “reno-vesico-sphincteric reflex”. The role of this reflex in urine transport requires further study. Received: 2 December 1997 / Accepted: 31 March 1998     

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.     

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.     

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.     

Effect of urethral dilation on vesical motor activity: identification of the urethrovesical reflex and its role in voiding

PURPOSE: We investigated the hypothesis that mild urethral distention, which presumably occurs during the passage of urine through the urethra, stimulates stretch receptors in the urethral wall, leading reflexively to vesical contraction. MATERIALS AND METHODS: We evaluated 9 male and 10 female healthy volunteers with a mean age +/- SD of 39.6 +/- 8.3 years. The posterior urethra was distended by a balloon filled with saline in 1 ml. increments up to 6 ml., while recording vesical pressure. The test was repeated after individual anesthetization of the urethra and bladder. RESULTS: Vesical pressure increased significantly at 1 and 2 ml. urethral distention (p <0.01). Increases in urethral distention effected further vesical pressure elevation (p <0.001), although there was no significant difference in distention at 3 to 6 ml. (p >0.05). No significant vesical pressure response of the individually anesthetized urethra or bladder occurred during urethral distention. CONCLUSIONS: Urethral distention is thought to cause vesical contraction through the stimulation of urethral stretch receptors. Vesical contraction at urethral distention postulates a reflex relationship that was abolished by individual anesthetization of the urethra and bladder. This relationship, which we call the urethrovesical reflex, appears to have a role in maintaining vesical contraction during voiding. Further studies are required to investigate the role of this reflex in voiding disorders.     

Effect of straining on perineal muscles and their role in perineal support: identification of the straining-perineal reflex

OBJECTIVE: The functional activity of the superficial (STPM) and deep (DTPM) transverse perineal muscles is poorly addressed in the literature. We investigated the hypothesis that these muscles act to support the perineum during increased intraabdominal pressure (IAP). METHODS: 46 healthy volunteers (mean age 30.4 +/- 1.2 y, 20 nulliparous women) were studied. The IAP was recorded by a manometric catheter introduced into the rectum. The response of the perineal muscles to straining (sudden by coughing and slow by Valsalva's maneuver) was registered by a needle electrode inserted into the STPM and DTPM separately. The response was recorded again after individual anesthetization of the perineal muscles and rectum using Xylocaine. The test was repeated using saline instead of Xylocaine and was performed on both sides. RESULTS: Straining (sudden or slow sustained) effected increase of the rectal pressure and the motor unit action potentials of both perineal muscles. The higher rectal pressure was increased by straining, the higher the motor unit action potentials increased MUAPs. The latency showed a gradual decrease upon incremental rectal pressure elevation. The perineal muscles did not respond to straining after individual anesthetization of the rectum and perineal muscles, but did respond to saline administration. The response was similar from muscles on both sides. CONCLUSIONS: Perineal muscle contraction on straining postulates a reflex relationship that we call the "straining-perineal reflex." We suggest that this reflex, which results in perineal muscle contraction, supports the perineum against the increased IAP induced by straining and the tendency of the perineum to descend. The results warrant further study of the role of the straining-perineal reflex in the genesis of perineal functional disorders.     

Positive bladder cooling reflex in patients with bladder outlet obstruction due to benign prostatic hyperplasia

The bladder cooling reflex was evaluated in patients with bladder outlet obstruction to study the effect of obstruction on the afferent neural function of the bladder, especially on the C-afferents. The bladder cooling test was performed by infusion of 0 °C saline into the bladder with simultaneous detrusor pressure measurement in 104 patients with bladder outlet obstruction due to benign prostatic hyperplasia. In 49 patients (47%) a positive cooling reflex was observed. This was defined as a rise in the detrusor pressure following cold saline instillation exceeding 15 cmH₂O (range 15–130 cmH₂O, mean 60.6 cmH₂O; positive group). In the remainder of cases the pressure rise ranged from 0 to 12 cmH₂O (mean 6.1 cmH₂O; negative group). Bladder outlet obstruction may cause some alteration in the afferent neural function of the bladder, in particular of the C-afferent fibers.     

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 distention inhibits the spinal micturition reflex via glycinergic or GABAergic mechanisms in rats with spinal cord injury

BACKGROUND: We examined the influence of rectal distention on the spinal micturition reflex and the mechanism underlying its inhibition of bladder contraction. METHODS: Fourteen conscious female Sprague-Dawley rats were used in this study after transection of the lower thoracic cord. Isovolumetric cystometry was performed before and after distention of the rectum by inflation of a rectal balloon, followed by intrathecal injection of strychnine (a selective glycine receptor antagonist) or bicuculline (a GABA(A) receptor antagonist) into the lumbosacral cord. RESULTS: Rectal distention (1.0-3.0 cm(3)) prolonged the interval, decreased the amplitude, and shortened the duration of bladder contraction, and eventually almost abolished bladder activity. After intrathecal injection of strychnine (0.001-10 microg) or bicuculline (0.001-1 microg) in animals with inhibition of bladder activity by rectal distention, the interval, amplitude, and duration of bladder contraction returned to baseline. CONCLUSION: These results suggest that there is an inhibitory rectovesical reflex in the lumbosacral cord of rats with spinal cord injury, which modulates the spinal micturition reflex via glycinergic or GABAergic mechanisms.     

Role of positive urethrovesical feedback in vesical evacuation. The concept of a second micturition reflex: the urethrovesical reflex

Upon feeling the urge to urinate, the urinary bladder contracts, the urethral sphincters relax and urine flows through the urethra. These actions are mediated by the micturition reflex. We investigated the hypothesis that vesical contraction is maintained by positive feedback through continuous flow of urine through the urethra, and that the cessation of urine flow aborts detrusor contraction. Normal saline was infused into the urinary bladders of 17 healthy volunteers (age 35.2 years±4.2(SD); ten women and seven men) at a rate of 100 ml/min. On urge, which occurred at a mean volume of 408.6 ml±28.7of saline, the subject micturated while the vesical and urethral pressures during voiding were being recorded; residual urine was measured. The test was repeated after anesthetizing the urethra with xylocaine gel or, on another occasion, after applying a bland gel . On micturition, the urine was evacuated as a continuous stream without straining; no residual fluid was collected. After urethral anesthetization, the fluid came out of the urethra in multiple intermittent spurts and only with excessive straining. There was a large amount of residual fluid (184.6 ml±28.4). The results of bland gel application showed no significant difference (P>0.05) from those without gel. Detrusor contraction during micturition is suggested to be maintained by positive urethrovesical feedback elicited by the continued passage of urine through the urethra. This feedback seems to be effected through the urethrovesical reflex, which produces vesical contraction on stimulation of the urethral stretch receptors. Abortion of this reflex by urethral anesthetization resulted in failure of detrusor contraction and excessive straining was needed to achieve bladder evacuation in multiple spurts. The urethrovesical reflex is thus assumed to constitute a second micturition reflex responsible for the continuation of detrusor contraction and urination. The role of this reflex in the pathogenesis of micturition disorders needs to be studied.     

The effect of external urethral sphincter contraction on the cavernosus muscles and its role in the sexual act

Objectives/Aim A study of the effect of external urethral sphincter contraction on ischio-/bulbo-cavernosus muscles could not be traced in the literature. We investigated the hypothesis that external urethral sphincter contraction induces cavernosus muscles’ contraction. Methods Twenty-one healthy volunteers (age 37.6 ± 9.7 SD years, 12 men, nine women) were studied. The electromyographic response of the ischio- and bulbo-cavernosus muscles to external urethral sphincter stimulation was recorded before and after anesthetization of the external urethral sphincter, and the ischio- and bulbo-cavernosus muscles; the response was also recorded using normal saline instead of lidocaine. Results Upon external urethral sphincter stimulation (five square pulses, 1 ms duration, 53.8 ± 10.2 mA threshold), both cavernosus muscles exhibited increased electromyographic activity with a mean amplitude of 386.2 ± 44.9 μV for the ischio-cavernosus and 318.4 ± 36.6 μV for the bulbo-cavernosus muscle. The mean latency read 16.8 ± 1.3 ms for the ischio-cavernosus muscle and 15.7 ± 1.2 ms for the bulbo-cavernosus muscle. Neither the ischio- nor the bulbo-cavernosus muscle responded to stimulation of the anesthetized external urethral sphincter, but both responded after saline administration. Likewise, the anesthetized ischio- and bulbo-cavernosus muscles showed no response to external urethral sphincter stimulation but responded after saline had been injected. Conclusions Increased electromyographic activity of the two cavernosus muscles on external urethral sphincter stimulation presumably denotes contraction of these two muscles and that this action is probably reflex, mediated through the ‘sphinctero-cavernosus-reflex’. Cavernosus muscles’ contraction assists in the erectile and ejaculatory mechanisms. It is suggested that this reflex be included as an investigative tool in the diagnosis of erectile and ejaculatory disorders, provided further studies are performed.     

The latissimus dorsi bladder myoplasty to assist detrusor function

The objective of this study was to evaluate whether an innervated skeletal muscle might augment detrusor function. In four dogs we performed the latissimus dorsi myoplasty, a transfer of the latissimus muscle as an innervated free flap wrapped around the bladder. Stimulation of the latissimus dorsi free flap initially achieved an average bladder pressure of 45.8 ± 8.41 cm H₂O, sufficient for partial evacuation. After 4 months the muscle generated a maximal pressure of 82 cm H₂O, resulting in an evacuation of 27.7%. For selected patients, the latissimus dorsi bladder myoplasty may provide an alternative to intermittent catheterization in the future. Received: 14 March 1997 / Accepted: 12 January 1998