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 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 micturition on the external anal sphincter: identification of the urethro-anal reflex

BACKGROUND/OBJECTIVE: A study on the response of the external anal sphincter (EAS) to the passage of urine through the urethra during micturition could not be found in the literature. We investigated the hypothesis that urine passage through the urethra effects EAS contraction to guard against possible flatus or stool leakage during micturition. METHODS: The study was performed in 23 healthy volunteers (age, 38.6 +/- 10.8 [SD] years; 14 men and 9 women). The EAS electromyogram (EMG) was performed during micturition by surface electrodes applied to the EAS. Also, the EAS EMG response to urethral stimulation by a catheter-mounted electrode was registered. The test was repeated after individual anesthetization of the EAS and urethra. RESULTS: The EAS EMG recorded a significant increase (P < 0.01) during micturition and on urethral stimulation at the bladder neck. Stimulation of the prostatic, membranous, or penile urethra produced no significant change in the EAS EMG. Urethral stimulation after individual EAS and urethral anesthetization did not cause any changes in the EAS EMG. CONCLUSIONS: Urine passing through the urethra or urethral stimulation at the vesical neck produced an increase in the EAS EMG, which presumably denotes EAS contraction, which seems to guard against flatus or fecal leakage during micturition. EAS contraction on urethral stimulation is suggested to be mediated through a urethro-anal reflex. Further studies on this issue may potentially prove the diagnostic significance of this reflex in micturition and defecation disorders.     

Role of positive anorectal feedback in rectal evacuation: the concept of a second defecation reflex: the anorectal reflex

BACKGROUND/OBJECTIVE: The present study investigated the hypothesis that rectal contraction is maintained by positive anorectal feedback elicited by continuous passage of stools through the rectal neck (anal canal), and that cessation of stool passage aborts rectal contraction. METHODS: Anal and rectal pressures were measured in 18 healthy volunteers (mean age = 38.6 years; 10 men, 8 women) during evacuation of saline infused into the rectum. Residual fluid volume was calculated. The test was repeated after separate application of lidocaine or bland gel to the rectal neck. RESULTS: On evacuation, fluid emanated from the rectal neck in continuous flow with no, or mild, straining. No residual saline was collected from 16 of 18 participants. After anal anesthetization, evacuation occurred in gushes induced with excessive straining; residual fluid was huge. Repetition of the test 2 hours after anesthetization produced the same results as before anesthetization. Bland gel applied to the rectal neck yielded results similar to those before gel application. CONCLUSION: Rectal contraction at defecation is suggested to be maintained by positive anorectal feedback evoked by continuous passage of stool through the rectal neck. This feedback appears to be affected through an anorectal excitatory reflex (ARR), which produces rectal contraction upon stimulation of anal stretch receptors. Abortion of this reflex by anal anesthetization seems to result in failure of the rectum to contract and in excessive straining to achieve rectal evacuation. ARR thus is suggested to be a second defecation reflex necessary to continue defecation, whereas the rectoanal inhibitory reflex is the primary reflex. The role of the ARR in pathogenesis of constipation and its utility in spinal cord injury need to be investigated.     

Micturitional Reflexes in Chronic Spinalized Cats: The Underactive Detrusor and Detrusor-Sphincter Dyssynergia

We studied micturitional reflexes in 46 unanesthetized adult male cats spinalized at C5-C6 17 to 125 days previously and in eight intact central nervous system chloralosed cats that were used as controls. Urethral pressure profiles, cystosphincterograms with the urethrovesical junction opened and closed, and mechanograms of detrusor and circular and longitudinal urethral muscles were performed. The effect of vesical, urethral, pelvic, or pudendal anesthesia and vesical and urethral mechanical stimulation were studied. Our results suggest that spinalization produces two major types of neurourologic disorders: (1) weakness of detrusor contractor reflexes (vesicovesical and urethrovesical contraction reflexes) and (2) exaggeration of urethral contractor reflexes (urethrourethral contraction reflex, guarding reflex). Secondarily the weakness of detrusor contractions diminishes the efficiency of the urethral reflex relaxation needed for voiding (vesicourethral relaxation reflex). Because of these abnormalities, two main syndromes appear: (1) underactive detrusor function and (2) detrusor sphincter dyssynergia. Isolated peripheral manipulations of the bladder or urethra do not improve micturition: (1) increase in detrusor contraction strength induces detrusor sphincter dyssynergia, and (2) relaxation of the external sphincter facilitates voiding, but urinary retention persists. It is proposed that spinalization produces a central micturitional dysreflexia responsible for the peripheral dysfunction, and treatment must be oriented toward the central dysreflexia rather than the peripheral dysfunction.     

Effect of Micturition on the External Anal Sphincter: Identification of the Urethro-Anal Reflex

Abstract

Background/Objective: A study on the response of the external anal sphincter (EAS) to the passage of urine through the urethra during micturition could not be found in the literature. We investigated the hypothesis that urine passage through the urethra effects EAS contraction to guard against possible flatus or stool leakage during micturition.

Methods: The study was performed in 23 healthy volunteers (age, 38.6 ± 10.8 [SD] years; 14 men and 9 women). The EAS electromyogram (EMG) was performed during micturition by surface electrodes applied to the EAS. Also, the EAS EMG response to urethral stimulation by a catheter-mounted electrode was registered. The test was repeated after individual anesthetization of the EAS and urethra.

Results: The EAS EMG recorded a significant increase (P < 0.01) during micturition and on urethral stimulation at the bladder neck. Stimulation of the prostatic, membranous, or penile urethra produced no significant change in the EAS EMG. Urethral stimulation after individual EAS and urethral anesthetization did not cause any changes in the EAS EMG.

Conclusions: Urine passing through the urethra or urethral stimulation at the vesical neck produced an increase in the EAS EMG, which presumably denotes EAS contraction, which seems to guard against flatus or fecal leakage during micturition. EAS contraction on urethral stimulation is suggested to be mediated through a urethra-anal reflex. Further studies on this issue may potentially prove the diagnostic significance of this reflex in micturition and defecation disorders.     

A study of the continence mechanism of the external urethral sphincter with identification of the voluntary urinary inhibition reflex

PURPOSE: The role of the external urethral sphincter in the opposition and interruption of the act of voiding was investigated. MATERIALS AND METHODS: The study included 7 men and 5 women with a mean age plus or minus standard deviation of 38.6 +/- 11.2 years. The bladder was filled with saline up to the urge sensation. Detrusor and posterior urethral pressures were recorded before and upon resisting the reflex detrusor contraction, and upon interrupting voiding by voluntary external urethral sphincter contraction. The test was repeated by interrupting the urinary stream with external urethral sphincter electrostimulation. The electromyography response of the internal urethral sphincter to the suppression and interruption of voiding was documented before and after internal urethral sphincter anesthetization. RESULTS: Suppression of the reflex detrusor contraction as well as of urinary stream interruption by external urethral sphincter contraction voluntarily or by electrostimulation resulted in a significant detrusor pressure decrease (p <0.01) and urethral pressure increase (p <0.001). Internal urethral sphincter electromyography activity, which normally disappears during voiding, was still present. After internalurethral sphincter anesthetization subjects suppressed the reflex detrusor contraction by voluntary external urethral sphincter contraction for a mean of 62.6 +/- 9.6 seconds, after which involuntary voiding occurred. The internal urethral sphincter showed no electromyography activity. CONCLUSIONS: The external urethral sphincter induces continence by preventing internal urethral sphincter relaxation at the detrusor contraction, which is suggested to be reflex in nature and is called the voluntary urinary inhibition reflex, and by mechanically compressing the urethra. Contraction of the external urethral sphincter, which is a striated muscle, mechanically occludes the urethra for a few seconds, by which time the detrusor has relaxed as an effect of the voluntary inhibition reflex.     

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.     

Overactive bladder inhibition in response to pelvic floor muscle exercises

A recent study by the senior author demonstrated that striated urethral sphincter contraction effected the inhibition of vesical contraction and suppression of the desire to micturate, an action suggested to be mediated through the "voluntary urinary inhibition reflex". We hypothesized that the effect of pelvic floor muscle (PFM) exercises on the overactive bladder was mediated through this reflex action. The current communication investigates this hypothesis. A total of 28 patients (mean age 44.8+/-10.2 years, 18 men, 10 women) with overactive bladder and 17 healthy volunteers (mean age 42.6+/-9.8 years, 12 men, 5 women) were enrolled in the study. The vesical and posterior urethral pressures were determined before and after vesical filling reached the volume at which urge in control subjects, and involuntary voiding in the patients, occurred. Intra-abdominal pressure was recorded to obtain detrusor pressure readings. The bladder was refilled to the above volume and the subject asked to hold PFM contractions for 10 s during which the vesical and posterior urethral pressures were recorded. In healthy volunteers, the mean detrusor and posterior urethral pressures at urge to void were 30.6+/-4.8 SD and 18.7+/-3.3 cm H(2)O, respectively. On PFM contraction, the detrusor pressure declined to 11.6+/-1.4 cm H(2)O (P<0.01) and urethral pressure increased to 139.8+/-17.4 cm H(2)O (P<0.001). In patients, the mean detrusor and posterior urethral pressure readings when the bladder was filled to the volume which induced involuntary incontinence, were 28.2+/-4.2 and 17.3+/-3.4 cm H(2)O, respectively; on PFM contractions, the detrusor pressure decreased to 10.6+/-2.1 cm H(2)O (P<0.01), while urethral pressure increased to 86.6+/-7.9 cm H(2)O (P<0.001) and voiding did not occur. In conclusion, PFM contractions led to a decline of detrusor and increase of urethral pressures and suppressed the micturition reflex. These contractions appear to induce their effect by preventing internal sphincter relaxation produced by the micturition reflex. Failure of the internal sphincter to relax seems to cause reflex detrusor relaxation, an action presumably mediated through the "voluntary urinary inhibition reflex". The results of the current study encourage the treatment of overactive bladder with PFM contractions.     

Role Of Positive Anorectal Feedback In Rectal Evacuation: The Concept Of A Second Defecation Reflex: The Anorectal Reflex

Abstract

Background/Objective: The present study investigated the hypothesis that rectal contraction is maintained by positive anorectal feedback elicited by continuous passage of stools through the rectal neck (anal canal), and that cessation of stool passage aborts rectal contraction.

Methods: Anal and rectal pressures were measured in 18 healthy volunteers (mean age = 38.6 years; 10 men, 8 women) during evacuation of saline infused into the rectum. Residual fluid volume was calculated. The test was repeated after separate application of lidocaine or bland gel to the rectal neck.

Results: On evacuation, fluid emanated from the rectal neck in continuous flow with no, or mild, straining. No residual saline was collected from 16 of 18 participants. After anal anesthetization, evacuation occurred in gushes induced with excessive straining; residual fluid was huge. Repetition of the test 2 hours after anesthetization produced the same results as before anesthetization. Bland gel applied to the rectal neck yielded results similar to those before gel application.

Conclusion: Rectal contraction at defecation is suggested to be maintained by positive anorectal feedback evoked by continuous passage of stool through the rectal neck. This feedback appears to be affected through an anorectal excitatory reflex (ARR), which produces rectal contraction upon stimulation of anal stretch receptors. Abortion of this reflex by anal anesthetization seems to result in failure of the rectum to contract and in excessive straining to achieve rectal evacuation. ARR thus is suggested to be a second defecation reflex necessary to continue defecation, whereas the rectoanal inhibitory reflex is the primary reflex. The role of the ARR in pathogenesis of constipation and its utility in spinal cord injury need to be investigated.     

Influence of temperature on urethra to bladder micturition reflex in the awake ewe

AIMS: The flow of fluid along the urethra is known to facilitate detrusor contraction during micturition. This reflex, previously described in awake ewes, helps to achieve complete bladder emptying. In anesthetized cats, another urethra to bladder reflex involving urethral cold receptors has been described. The aim of this study was to investigate whether the urethral reflex first described in awake ewes could also be temperature-dependent. METHODS: Experiments were performed on 10 healthy ewes. Urethral flows were performed by injecting 10 ml saline (ranging from 17 to 43 degrees C) at the level of the proximal urethra. Catheterization of the bladder was performed so that detrusor pressure was continually recorded during the experiments. RESULTS: Urethral flows using body temperature saline (37-39 degrees C) consistently evoked detrusor contraction. Urethral flows using saline at temperatures between 40 and 43 degrees C induced detrusor contractions that were not significantly different from those observed at 37-39 degrees C. Urethral flows using saline at temperatures below 37-39 degrees C (17-36 degrees C) resulted in a weaker or absent detrusor contraction. CONCLUSIONS: In ewes, we have shown that urethral to bladder micturition reflex involving mechanoreceptors is decreased at temperatures below the physiological range. It is suggested that transient receptor potential vanilloid cation channels (e.g., TRPV4 which is activated by sheer/stress flows at near-body temperature) could be involved in this urethra to bladder reflex. In humans, this reflex has hardly been described and is still a matter of debate. Our results reinforce that its full investigation may require systematic use of a range of saline flows at different temperatures.     

Urethral response during bladder contraction induced by subcutaneous bethanechol chloride: elicitation of a sympathetic reflex urethral constriction

The responses of the urethra to bladder filling and to subcutaneous bethanechol were studied in a surgically separated bladder-urethra preparation in chloralose anesthetized cats. With the pudendal nerves cut or the neuromuscular junction blocked with gallamine, urethral closure pressure increased during bladder filling and the initial phase of the micturition contraction. It then fell spontaneously or in response to bladder emptying through a vent. With the bladder volume held constant subcutaneous bethanechol induced an increase in basal bladder pressure which culminated in a sustained (reflex) contraction. The urethral constrictor response resembled that seen during the cystometrogram; an increase during the rise in detrusor pressure and a fall during the latter part of the sustained (reflex) contraction. In both cases the urethral response was substantially depressed by hypogastric nerve transection or by intravenous prazosin, implying that the urethral responses were reflexly mediated through the sympathetic system. Intra-arterial bethanechol also produced a urethral constriction, but this response was abolished by atropine and not affected by hypogastric nerve section or prazosin. It is therefore concluded that although bethanechol can produce urethral constriction through a direct muscarinic action on the urethra, it does not do so after subcutaneous administration in a neurally intact cat. The urethral response seen after subcutaneous bethanechol administration is part of the micturition reflex complex and is sympathetically mediated.     

Residual urine,underactive detrusor function,and the nature of detrusor/sphincter dyssynergia

In a group of 280 patients with mixed pathology the adequacy of the detrusor contraction during voiding has been assessed by a new method. For the group as a whole, residual urine is nearly always the result of the fading away of the detrusor contraction and rarely of premature sphincter contraction. It is strongly associated with failure to attain an adequate detrusor contraction at any time during the micturition. The same is true both for children who show consistent urethral overactivity during voiding and for patients with detrusor/sphincter dyssynergia of neuropathic origin. The results suggest that in detrusor/sphincter dyssynergia or other types of urethral overactivity, it may be misleading to ascribe inefficient bladder emptying solely to the obstructive effect of the urethral closure mechanism; the underactive detrusor function should also be taken into account. Often there appears to be an incomplete activation of the micturition reflex, resulting in both incomplete stimulation of the detrusor and incomplete relaxation of the urethral closure mechanism.     

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.     

Levator-urethral reflex. A new reflex with clinical significance

A preliminary study of a new reflex which I called "levator-urethral reflex" is presented. Twenty-three volunteers were studied. Two concentric needle electrodes were introduced: one in the levator ani muscle (stimulating electrode) and the other in the external urethral sphincter (recording electrode). Levator stimulation evoked external sphincter contraction in all the subjects. The anesthetized sphincter did not respond while the saline-infiltrated one responded. The mean latency of the reflex was 168 ms. The levator-urethral reflex regulates the relation between micturition and continence. Reflex external urethral sphincter contraction keeps micturition under control despite the involuntary opening of the vesical neck as a result of levator contraction. Measurement of the latency of the reflex could be an objective and accurate means of investigating micturition disorders.     

URETHRAL AFFERENT NERVE ACTIVITY AFFECTS THE MICTURITION REFLEX; IMPLICATION FOR THE RELATIONSHIP BETWEEN STRESS INCONTINENCE AND DETRUSOR INSTABILITY

PURPOSE: A causative relationship between stress urinary incontinence (SUI) and detrusor instability has been suspected but never proven. Many women with mixed incontinence have resolution of detrusor instability after surgical correction of SUI. We sought experimental support that stimulation of urethral afferent nerves can induce or change reflex detrusor contractions. MATERIALS AND METHODS: Urethral perfusion pressure and isovolumetric bladder pressure were measured with catheters inserted through the bladder dome in urethane anesthetized female S.D. rats (250 to 300 grams; n = 12). The catheter assembly was seated securely in the bladder neck to block passage of fluid between the bladder and urethra without affecting the nerve supply to the organs. The external urethra was not catheterized. Responses were examined in the control state at a urethral saline perfusion speed of 0.075 ml. per minute. Intraurethral drugs were administered following blockade of striated sphincter activity with intravenous alpha-bungarotoxin (0.1 mg./kg.). RESULTS: Stopping the urethral saline infusion caused a significant decrease in micturition frequency in approximately 50% of the animals studied (n = 12). Intraurethral lidocaine (1%) infused at 0.075 ml. per minute caused a slight decrease in urethral perfusion pressure but no change in detrusor contraction amplitude. However, intraurethral lidocaine caused a significant (45%) decrease in the bladder contraction frequency (n = 5). The micturition frequency returned to baseline 30 minutes after stopping lidocaine infusion. Intraurethral infusion of nitric oxide (NO) donors (S-nitroso-N-acetylpenicillamine [SNAP] (2 mM) or nitroprusside (1 mM) immediately decreased urethral perfusion pressure by 30 to 37% (n = 5). A 45 to 75% decrease (n = 5) in bladder contraction frequency was also seen, which was similar to that observed following lidocaine. Neither NO donor changed the amplitude of bladder contractions. CONCLUSIONS: These results indicate that in the anesthetized rat activation of urethral afferents by urethral perfusion can modulate the micturition reflex. Thus in patients with stress urinary incontinence, leakage of urine into the proximal urethra may stimulate urethral afferents and facilitate voiding reflexes. This implies that stress incontinence can induce and/or increase detrusor instability. These findings have significant implications for the treatment of patients with mixed urge and stress incontinence. Correction of stress incontinence by surgery or pelvic floor exercise in patients with mixed incontinence may resolve the detrusor instability.     

Bladder instability in women: A premature activation of the micturition reflex

Urethrocystometry was performed during a provocative hand washing test in 163 patients, 115 of whom had a prior history of urge incontinence. Almost invariably, a rise in detrusor pressure, when present, followed a fall in urethral pressure, and both were preceded by urge symptoms. This pattern appears to conform to the concept of “urethral instability”, “detrusor instability” and urge incontinence being different manifestations of a prematurely activated micturition reflex.     

Urethral sphincters response to cavernosus muscles stimulation with identification of cavernoso-urethral reflex

The functional activity of the urethral sphincters during cavernosus muscles' contraction at coitus has been poorly addressed in the literature. We investigated the hypothesis that cavernosus muscles' contraction affects reflex contraction of the urethral sphincters to guard against semen reflux into the urinary bladder or urine leakage from the bladder during orgasm and ejaculation. The electromyographic (EMG) response of the external (EUS) and internal (IUS) urethral sphincters to ischio- (ICM) and bulbo- (BCM) cavernosus muscle stimulation was studied in 15 healthy volunteers (9 men, 6 women, age 39.3 +/- 8.2 SD years). An electrode was applied to each of ICM and BCM (stimulating electrodes) and the 2 urethral sphincters (recording electrodes). The test was repeated after individual anesthetization of the urethral sphincters and the 2 cavernosus muscles, and after using saline instead of lidocaine. Upon stimulation of each of the 2 cavernosus muscles, the EUS and IUS recorded increased EMG activity. Repeated cavernosus muscles' stimulation evoked the urethral sphincteric response without fatigue. The urethral sphincters did not respond to stimulation of the anesthetized cavernosus muscles nor did the anesthetized urethral sphincters respond to cavernosus muscle stimulation. Saline infiltration instead of lidocaine did not affect the urethral sphincteric response to cavernosal muscle stimulation. Results were reproducible. Cavernosus muscles' contraction is suggested to effect EUS and IUS contraction. This action seems to be reflex and mediated through the 'cavernoso-urethral reflex.' Urethral sphincters contraction upon cavernosus muscles contraction during sexual intercourse presumably prevents urine leak from the urinary bladder to urethra, prevents retrograde ejaculation, and propels ejaculate from the posterior to the penile urethra. The cavernoso-urethral reflex can act a diagnostic tool in the investigations of patients with ejaculatory disorders.     

Effect of micturition on clitoris and cavernosus muscles: an electromyographic study

We investigated the hypothesis that passage of urine through urethra stimulates corporal tissue and cavernosus muscles. Electromyographic (EMG) activity of corpora cavernosa (CC), bulbocavernosus muscle (BCM), and ischiocavernosus muscle (ICM) was recorded in 27 healthy women before and during micturition. These tests were repeated after individual anesthetization of urethra, corporal tissue, and cavernosus muscles. During micturition, slow wave variables of CC decreased and motor unit action potentials of the BCM and ICM increased. These EMG changes returned to basal values on micturition interruption or termination. Micturition after individual anesthetization of the urethra, corporal tissue, and cavernosus muscles did not effect significant changes in these structures. Decreased EMG activity of CC and increased activity of cavernosus muscles during micturition apparently denotes corporal tissue relaxation and cavernosus muscles’ contraction. The latter two actions occurring on micturition are suggested to be mediated through a reflex called “urethro-corporocavernosal reflex” and effect a mild degree of clitoral tumescence.     

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.