Rise In Bladder Pressure Research Articles

Is isolated bladder outlet obstruction associated with hydronephrosis? A database analysis.

To examine whether isolated bladder outlet obstruction in the absence of associated lower urinary tract abnormality results in hydronephrosis. Isolated obstruction causes a brief rise in bladder pressure that might not trigger hydronephrosis. Data included adult men who underwent urodynamics for refractory non-neurogenic lower tract symptoms between 2011 and 2020. International Continence Society indices for obstruction (bladder outlet obstruction index [BOOI] ≥ 40) and underactivity (bladder contractility index [BCI] < 100) were calculated. Storage abnormality was defined as detrusor overactivity (DO) or poor compliance (<20 ml/cm H2 0). Isolated obstruction was defined as BOOI ≥ 40, BCI ≥ 100 and no storage abnormality. Nonparametric tests using R program (3.5.0) applied (p < .05 significant). Logistic regression analyses were performed to study the relationships of hydronephrosis with lower urinary tract function. A total 1596 men (range, 18-91 years; median, 51.0 years; Q3, 64.0 years; Q1, 34.0 years) were eligible. Hydronephrosis was noted in 274 (17.2%). A total of 45.4% were obstructed, 52.3% were underactive and 41.7% had storage abnormality. Storage abnormality (odds ratios [OR], 2.05; 95% confidence interval [CI]: 1.56, 2.69; p < .001) and bladder contractility (OR, 1.68; 95% CI, 1.25-2.26; p < .001) but not obstruction (OR, 1.07; 95% CI, 0.80-1.44; p = .634) was associated with hydronephrosis. Of eight possible combinations, men with BOO ≥ 40, BCI ≥ 100 and storage abnormality had highest probability of hydronephrosis (OR, 0.29; 95% CI, 0.24-0.33). Subanalysis showed that poor compliance (OR, 3.39; 95% CI, 2.49-4.60; p < .001) but not DO was associated with hydronephrosis. Younger age and higher postvoid residual urine were also associated with hydronephrosis. In adult men with refractory non-neurogenic lower urinary tract symptoms, isolated bladder outlet obstruction is not associated with hydronephrosis.

Afferent Nerve Activity Ex Vivo and Voiding Frequency In Vivo are Driven by Bladder Filling Rate in a Mouse Model of Polydipsia‐Polyuria

The mechanisms regulating urinary voiding function are not entirely understood. Many disorders of the lower urinary tract such as overactive bladder, urinary incontinence, and underactive bladder are associated with dysfunctional voiding behavior. Developing treatments to improve voiding function in afflicted individuals has proved to be problematic, in part due to a lack of basic understanding of the mechanisms responsible for controlling voiding function.We have shown previously in an ex vivo bladder model that afferent nerve activity increases as the bladder is filled. Furthermore, transient pressure events occurring during bladder filling trigger substantial rises in afferent nerve activity, more so than would occur during a similar rise in bladder pressure associated with bladder filling. This observation suggests that localized wall deformations associated with transient pressure events could transduce important sensory information to the central nervous system as to the filling state of the bladder. In the present study, we hypothesized that bladder filling rate is an important parameter that controls voiding function in vivo. We used an acute sucrose induced polydipsia/polyuria model that allows us to determine the impact of bladder filling rate on voiding behavior noninvasively in conscious freely moving mice.Male C57Bl6 mice (6 weeks old) were placed into a UroVoid apparatus for 48 hour voiding studies. One group of mice had access to tap water while a second group of mice had access to 5% sucrose in water. All mice had access to standard rodent chow. The UroVoid apparatus allows us to quantify the time and volume for each micturition.Mice drinking 5% sucrose consumed substantially more fluid than mice consuming tap water (26.98 ± 13.12 ml vs. 7.23 ± 1.35 ml). This polydipsia was reflected in a profound polyuria in mice consuming sucrose, as these mice voided a total of 18.98 ± 13.52 ml of urine over 79 ± 42 voids compared to 3.91 ± 0.54 ml of urine over 22 ± 16 voids in mice consuming tap water. Using the voided urine volume and the intermicturition interval for each void, we calculated that the urine production rate (UPR) is ~2 μl/min in mice consuming tap water, whereas the UPR is greatly elevated to ~25 μl/min in mice consuming 5% sucrose. Voiding frequency is greatly increased in mice consuming 5% sucrose, which we believe reflects underlying sensory function.To address the impact of bladder filling rate on sensory function, we measured afferent pelvic nerve activity in ex vivo bladder preparations at filling rates of 3.3, 10, and 30 μl/min. As expected, sensory nerve activity was increased at higher filling rates. For example, at an intravesical pressure of 15–20 mmHg, afferent nerve frequency increased from 91.5 ± 43.0 Hz at 3.3 μl/min to 174.9 ± 64.1 Hz at 30 μl/min.In conclusion, sucrose‐induced polydipsia/polyuria in mice is an effective way to examine the impact of bladder filling rate on voiding behavior. Increases in bladder filling rate are associated with increases in afferent nerve outflow in the bladder, and this increase in sensory outflow may contribute to elevated voiding frequency at higher bladder filling rates.Support or Funding InformationSupported by NIH R37 DK053832

Suppression of Urinary Voiding “on Demand” by High-Frequency Stimulation of the S1 Sacral Nerve Root in Anesthetized Rats

High-frequency (kHz) stimulation of preganglionic pelvic nerve afferents can inhibit voiding in both anesthetized and conscious rats. The afferents travel via the S1 sacral nerve root, which is easier to access than the distal pelvic nerve fibers within the abdominal cavity. We therefore investigated whether voiding could be inhibited by high-frequency stimulation at S1 and how this compared to distal pelvic nerve stimulation. Urethane-anesthetized rats were instrumented to record bladder pressure and abdominal wall electromyogram and to stimulate the distal preganglionic pelvic nerve bundle and S1 sacral root. Saline was infused continuously into the bladder to evoke repeated voiding. Stimulation was initiated within 1-2 sec of the onset of the steep rise in bladder pressure signaling an imminent void. In six rats, stimulation of the distal pelvic nerve bundle (1-3 kHz sinusoidal waveform 1 mA, 60 sec) supressed the occurrence of an imminent void. Voiding resumed within 70 ± 13.0 sec (mean ± SEM) of stopping stimulation. Stimulation (using the same parameters) of the S1 root at the level of the sacral foramen suppressed voiding for the entire stimulation period in three rats and deferred voiding for 35-56 sec (mean 44.0 ± 3.2 sec) in the remaining three. Stimulation at either site when the bladder was approximately half full, as estimated from previous intervoid intervals, had no effect on voiding. This preliminary study provides proof-of-concept for the sacral root as an accessible target for high-frequency stimulation that may be developed as an "on demand" neuromodulation paradigm to suppress unwanted urinary voids. The authors reported no conflict of interest.

Suppression of Urinary Voiding by Conditional High Frequency Stimulation of the Pelvic Nerve in Conscious Rats.

Female Wistar rats were instrumented to record bladder pressure and to stimulate the left pelvic nerve. Repeated voids were induced by continuous infusion of saline into the bladder (11.2 ml/h) via a T-piece in the line to the bladder catheter. In each animal tested (n = 6) high frequency pelvic nerve stimulation (1–3 kHz, 1–2 mA sinusoidal waveform for 60 s) applied within 2 s of the onset of a sharp rise in bladder pressure signaling an imminent void was able to inhibit micturition. Voiding was modulated in three ways: (1) Suppression of voiding (four rats, n = 13 trials). No fluid output or a very small volume of fluid expelled (<15% of the volume expected based on the mean of the previous 2 or 3 voids). Voiding suppressed for the entirety of the stimulation period (60 s) and resumed within 37 s of stopping stimulation. (2) Void deferred (four rats, n = 6 trials). The imminent void was suppressed (no fluid expelled) but a void occurred later in the stimulation period (12–44 s, mean 24.5 ± 5.2 s after the onset of the stimulation). (3) Reduction in voided volume (five rats, n = 20 trials). Voiding took place but the volume of fluid voided was 15–80% (range 21.8–77.8%, mean 45.3 ± 3.6%) of the volume expected from the mean of the preceding two or three voids. Spontaneous voiding resumed within 5 min of stopping stimulation. Stimulation during the filling phase in between voids had no effect. The experiments demonstrate that conditional high frequency stimulation of the pelvic nerve started at the onset of an imminent void can inhibit voiding. The effect was rapidly reversible and was not accompanied by any adverse behavioral side effects.

High Frequency Stimulation of the Pelvic Nerve Inhibits Urinary Voiding in Anesthetized Rats

Urge Urinary Incontinence: “a sudden and uncontrollable desire to void which is impossible to defer” is extremely common and considered the most bothersome of lower urinary tract conditions. Current treatments rely on pharmacological, neuromodulatory, and neurotoxicological approaches to manage the disorder, by reducing the excitability of the bladder muscle. However, some patients remain refractory to treatment. An alternative approach would be to temporarily suppress activity of the micturition control circuitry at the time of need i.e., urgency. In this study we investigated, in a rat model, the utility of high frequency pelvic nerve stimulation to produce a rapid onset, reversible suppression of voiding. In urethane-anesthetized rats periodic voiding was induced by continuous infusion of saline into the bladder whilst recording bladder pressure and electrical activity from the external urethral sphincter (EUS). High frequency (1–3 kHz), sinusoidal pelvic nerve stimulation initiated at the onset of the sharp rise in bladder pressure signaling an imminent void aborted the detrusor contraction. Urine output was suppressed and tone in the EUS increased. Stimulating the right or left nerve was equally effective. The effect was rapid in onset, reversible, and reproducible and evoked only minimal “off target” side effects on blood pressure, heart rate, respiration, uterine pressure, or rectal pressure. Transient contraction of abdominal wall was observed in some animals. Stimulation applied during the filling phase evoked a small, transient rise in bladder pressure and increased tonic activity in the EUS, but no urine output. Suppression of micturition persisted after section of the contralateral pelvic nerve or after ligation of the nerve distal to the electrode cuff on the ipsilateral side. We conclude that high frequency pelvic nerve stimulation initiated at the onset of an imminent void provides a potential means to control urinary continence.

Study of the occurrence of intra-abdominal hypertension and abdominal compartment syndrome in patients of blunt abdominal trauma and its correlation with the clinical outcome in the above patients.

BackgroundIntra-abdominal pressure (IAP) measurements have been identified as essential for diagnosis and management of both intra-abdominal hypertension (IAH) and Abdominal compartment syndrome (ACS). It has gained prominent status in ICUs worldwide. We aimed to evaluate the utility of measurement of rise in bladder pressure to assess IAP levels in blunt abdominal trauma (BAT) patients.Patients and methodsThirty patients of BAT with solid organ injuries were included in this study. Intra-abdominal pressure was measured through a Foleys bladder catheter throughout their stay. Bladder pressure was compared with clinical parameters like mean arterial pressures(MAP), respiratory rate(RR), serum creatinine(SC) and abdominal girth(AG) and also with outcome in terms of intervention whether operative(OI) or non-operative(NOI).ResultsBladder pressure showed significant correlation with MAP (R = −0.418; P = 0.022), AG (R = 0.755; P = 0.000), SC (R = 0.689; P = 0.000) and RR (R = 0.537; P = 0.002). Bladder pressure (R = 0.851; P = 0.000), SC (R = 0.625; P = 0.000), MAP (R = −0.350; P = 0.058) and maximum AG difference (R = 0.634; P = 0.000) showed significant correlation with intervention. In total, 17 patients (56 %) required intervention, 9 patients (30 %) underwent NOI (pigtailing or aspiration) while 8 (27 %) needed OI. More than 3 derailed parameters were associated with 100 % intervention (Mean 3.47, SD-1.23). High APACHE III score on admission (>40) was associated with increased intervention (p = 0.001). Intervention correlates well with Grade of injury (p = 0.000) and not with number of organs injured (p = 0.061). Blood transfusion of 2 or more units of blood was associated with increased intervention (p = 0.000).ConclusionIncreased bladder pressure and other clinical parameters (MAP, SC, RR and change in AG) correlates well with intervention. Elevated bladder pressure correlates well with other clinical parameters in patients with BAT. Bladder pressure, SC, MAP, RR and AG difference can be used to determine the group of patients that can be managed conservatively and those that would benefit with minimal intervention or exploration. During Non-operative management (NOM) of patients with BAT and multiple solid organ injuries, IAP monitoring may be a simple and objective guideline to suggest further intervention whether NOI or OI. Although routine bladder pressure measurements will result in unnecessary monitoring of large number of patients it is hoped that patients with IAH can be detected early and subsequent ACS with morbid abdominal exploration can be prevented. However the criterion for non-operative failure and the point of decompression needs further refinement to prevent an increase of nontherapeutic operations.

Management of Low Compliant Bladder in Spinal Cord Injured Patients.

Low bladder compliance means an abnormal volume and pressure relationship, and an incremental rise in bladder pressure during the bladder filling. It is well known that at the time bladder capacity decreases, intravesical pressure increases, and the risk of upper deterioration increases. Hypocompliance is usually thought to be the range from 1.0 to 20.0 mL/cmH2 O. Though the exact cause of hypocompliance is not known, it may be caused by changes in the elastic and viscoelastic properties of the bladder, changes in detrusor muscle tone, or combinations of the two. Management aims at increasing bladder capacity with low intravesical pressure. The main is a medical therapy with antimuscarinics combined with clean intermittent catheterization. The results are sometimes unsatisfactory. Various drugs or agents through the mouth or the bladder, including oxybutynin, new antimuscarinics, capsaicin and resiniferatoxin were tried. Among them botulinum toxin-A is promising. Some patients eventually required surgical intervention in spite of the aggressive medical therapy. Finally most patients undergo the surgical treatment including autoaugmentation, diversion, and augmentation cystoplasty. Among them augmentation cystoplasty still seems the only clearly verified treatment method.

78 Use of a rabbit model to investigate the feasibility of using an innervated neosphincter transplant for the treatment of stress urinary incontinence.

Aim: To examine the feasibility of using an innervated smooth muscle wrap as a neosphincter in a rabbit model of urinary incontinence.Methods: Rabbits were rendered incontinent surgically by lesion of the proximal urethral wall to the level of the submucosa (n = 20). In twelve animals a strip of dartos smooth muscle was wrapped around the lesioned urethra to create a new urethral sphincter and stimulating electrodes were inserted into the muscle. After a recovery period of at least one‐week cystometrograms were established for control (urethra intact), lesioned and lesion plus neosphincter animals.Results: Infusion of saline into the bladder of control animals caused a slow rise in bladder pressure until, at approximately 20–30 ml, there was an increase in pressure that rose steeply and was associated with bladder emptying. The threshold for this reflex emptying was 2–3 cm H2O, and the maximum pressure during the reflex was 6–15 cm H2O. After the bladder emptied, the pressure dropped to 0–2 cm H2O. In rabbits with lesioned sphincters, it was not possible to obtain a normal cystometrogram because there was leakage of fluid from the urethral opening before a volume and pressure sufficient to elicit a reflex was achieved. The loss of the majority of fluid often occurred without a significant pressure increase, that is, there was no true emptying reflex. Similar results were observed in animals in which the urethra had been lesioned and implanted with the smooth muscle neosphincter. Prior to electrical stimulation of the neosphincter, with constant current pulses at 2 Hz, substantial leak occurred at 11.4 ± 2.5 ml, whereas during stimulation voiding occurred at 17.8 ± 1.4 ml. At void or emptying, the peak pressure was 6.1 ± 0.1 cm H20 in control, 0.7 ± 0.2 in operated but not stimulated and 3.5 ± 0.6 in the same animals during stimulation. A satisfactory improvement of continence was observed for a period of up to 6½ months postsurgery. At the end of the study, histological examination confirmed the neosphincter to be both healthy and viable.Conclusion: Smooth muscles of the dartos display contractile properties which make them suitable for use as transplantable sphincters. A smooth muscle neosphincter, controlled by electrical stimulation, can restore continence after urethral damage.

Alteration of collagen three-dimensional architecture in noncompliant human urinary bladder.

Urinary bladder compliance refers to the change in bladder pressure in response to variations in bladder volume. The normal bladder is able to accommodate large volumes of urine with minimal changes in pressure. In the laboratory setting, the normal rise in bladder pressure is less than 6 to 10 cm H2O34. Loss of bladder compliance is reflected by a stiff, inelastic bladder that experiences a rapid rise in pressure during bladder filling. Pressures exceeding 40 cm H2O result in deterioration of the upper urinary tract.23 Loss of compliance is seen with a variety of disease states, both congenital and acquired, which result in a functional or mechanical bladder outlet obstruction (Table 1).

Effect on urinary bladder function and arterial blood pressure of the activation of putative purine receptors in brainstem areas.

The effect on bladder function and arterial blood pressure of adenosine-5′-triphosphate (ATP) and its synthetic analogue, α,β-methylene ATP (α,β-meATP) applied by microinjection to brainstem areas was assessed in the anaesthetised, paralysed and artificially ventilated female rat. Recordings of bladder pressure, changes in the pelvic nerve activity, arterial blood pressure and heart rate were evaluated. The purinergic drugs were microinjected into two brainstem areas – the periaqueductal grey matter (PAG) and the area of the Barrington nucleus/locus coeruleus (LC) – only after electrical stimulation (50 Hz, 1 ms, 30–50 μA; n (PAG)=17; n (LC)=18) and the microinjection of glutamate (2 mM, pH 7.4±0.1; n (PAG)=16; n (LC)=16) had shown increases of bladder pressure and/or rate of bladder contractions and/or pelvic nerve activity at specific sites. Electrical and glutamate activation of PAG evoked an increase of arterial blood pressure. Microinjections of ATP (20 mM, pH 7.4±0.1; n (PAG)=11; n (LC)=11) and α,β-meATP (2 mM, pH 7.4±0.1; n (PAG)=10; n (LC)=9) both evoked consistent increases of bladder pressure and/or pelvic nerve activity. Stimulation with ATP elicited a biphasic change of arterial blood pressure characterised by an increase followed by a decrease which was accompanied by a rise of heart rate. Microinjection of α,β-meATP into PAG did not elicit a consistent response: a decrease of arterial blood pressure was evoked in five rats, while in two other rats an increase occurred. Electrical stimulation and glutamate activation of Barrington’s nucleus/LC evoked an increase of arterial blood pressure, but a decrease was observed after microinjection of both ATP and α,β-meATP. At some sites ( n=8) the effect of α,β-meATP after a pre-injection at the same site of the P2 purino receptor antagonist, suramin (20 mM, pH 7.4±0.1) was smaller than the control. At three sites within PAG and two within LC located more medially to sites where an excitatory response had been observed, electrical stimulation evoked a small decrease or no change in bladder pressure. Following the stimulus, a rise in bladder pressure was preceded by an increase of pelvic nerve activity. A similar effect of glutamate was observed in one case. These data suggest that activation of P2 purine receptors in both PAG and Barrington’s nucleus/LC is implicated in the neuronal mechanisms that generate patterns of activity in the parasympathetic innervation of the bladder and that purines also act at this level to modify sympathetic outflow to the cardiovascular system.

Neural Control of Urethral Outlet Activity in Vivo: Role of Nitric Oxide

The present study investigated the role of nitric oxide (NO) in the reflex changes in urethral outlet activity during micturition. Isovolumetric bladder contractions, urethral pressure and external urethral sphincter electromyogram (EUS EMG) activity were recorded independently in urethane-anesthetized rats. During reflex bladder contractions, the urethra exhibited reflex responses characterized by an initial decrease in urethral pressure in conjunction with a rise in bladder pressure. This was followed by a period of high frequency oscillations (HFOs) associated with maximal urethral relaxation and burst type EUS EMG activity. Administration of N-nitro-L-arginine (L-NOARG) 10 mg./kg. intravenously, a nitric oxide synthase inhibitor, reversibly decreased the magnitude (62 percent, p less than 0.05) and duration (40 percent, p less than 0.05) of reflex urethral relaxation (N = 7). In 4 additional experiments, L-NOARG (10 to 15 mg./kg. intravenously) completely eliminated reflex urethral relaxation during micturition, and this effect was reversed in all animals by the administration of L-arginine (100 to 150 mg./kg. intravenously). Administration of N-nitro-D-arginine (D-NOARG) (10 to 30 mg./kg. intravenously) had no effect on reflex urethral relaxation. Neuromuscular blockade (vecuronium bromide 5 mg./kg. intravenously) reversibly decreased resting urethral pressure and eliminated the HFOs. The urethral smooth muscle relaxation that remained after neuromuscular blockade was eliminated following administration of L-NOARG (10 mg./kg. intravenously) in 2 of 3 animals. These results suggest that reflex urethral responses during micturition involve changes in both smooth and striated muscle activity, and that the predominant neurotransmitter mechanisms that mediate reflex urethral smooth muscle relaxation involve NO.

Micturition in the unanesthetized rat: effects of intrathecal capsaicin, N-vanillylnonanamide, 6-hydroxydopamine and 5,6-dihydroxytryptamine

Unanesthetized rats chronically implanted with vesical and intrathecal catheters were injected intrathecally (i.t.) with either capsaicin (CAP), N-vanillylnonanamide (VN), 6-hydroxydopamine (6-OHDA), or 5,6-dihydroxytryptamine (5,6-DHT). The volume-evoked micturition reflex was assessed by cystometrography before, and 2 h, 1 day and 7 days after injection. In control and vehicle-injected rats, the infusion of saline into the bladder resulted in a periodic contraction of the bladder with synergic sphincter relaxation. One day after i.t. CAP and VN (70 μg each), 50% and 30% of the animals displayed a blockade of the micturition reflex, respectively. In these animals, the infusion of saline resulted in a gradual rise in bladder pressure up to a plateau (overflow pressure) equivalent to the predrug bladder opening pressure. When the plateau was reached, continuous dribbling of urine with no bladder contractions was observed. Most of the affected rats displayed some micturition responses by day 7. Following i.t. injection of 5,6-DHT (20 μg) or 6-OHDA (20 μg), the micturition reflex displayed small but significant increases in bladder volume with no changes in pressure profile. Small primary afferents, sensitive to the neurotoxic effects of CAP and VN appear to play a major tonic role in the regulation of the micturition reflex in unanesthetized rats. Serotonergic and adrenergic descending pathways might play a role in the maintenance of resting bladder tone.

6 Urinary incontinence

The last decade has seen a marked improvement in our understanding of the pathophysiology of urinary incontinence in the elderly. We are now able to manage this problem much more effectively. The changes responsible for the development of urinary incontinence in the elderly are complex. There is no doubt that some aspects of ageing of the lower urinary tract are yet to be fully understood. Much of the work conducted to date involves cross-sectional sampling of populations with comparison between age groups (Carlile et al, 1987). If a difference exists between the elderly and the young sampled, however, it is not necessarily valid to attribute this to the ageing process: differences may have been induced by intercurrent illnesses or environmental influences. To obtain data on the changes genuinely induced by the ageing process requires longitudinal studies following people as they grow old--logistically this type of work is extraordinarily difficult to perform. In consequence the data that we do have from longitudinal studies comes from animal experiments, chiefly in mice (Phillips and Davies, 1980). It is difficult to feel confident about extrapolating the conclusions from these experiments to humans. Nevertheless we find that the elderly do exhibit different patterns of disease from those of the young. All that we can say about these observations is that they appear to be associated with old age while not necessarily being caused by natural ageing. The detrusor muscle is a remarkably organized structure which is capable of a number of intricate functions. During filling of the bladder the detrusor relaxes as the bladder wall distends so that a virtually constant minimal pressure is maintained. The sensation of bladder fullness is transmitted to the consciousness when appropriate and not before. Contraction of the detrusor is voluntarily induced and results in a rise in bladder pressure, a closure of the ureteric orifices and opening of the bladder neck. The voiding detrusor contraction is closely coordinated with urethral sphincter relaxation and the whole process of voiding is carefully sustained until complete bladder emptying. A breakdown in one or more of these functions may lead to urinary incontinence. Much of the normal behaviour of the bladder and urethra is dependent on complex neurological controls. Because the nervous system is particularly susceptible to age-related degenerative changes, it should be no surprise to

The effects of parasympathetic blocking agents on bladder electromyograms and function in conscious and anaesthetized cats

Voiding induced in conscious cats by infusion of sterile saline into the bladder via a chronically implanted bladder catheter was stable over many months. Artefact-free recordings of electrical activity obtained from the bladder neck and dome of these preparations during bladder filling and voiding showed characteristic voiding electromyograms but did not permit a functional differentiation. Both voiding and the associated electromyogram were abolished by the ganglion blocking agent, pentolinium. Hyoscine or methyl atropine did not affect the electromyogram but impaired the ability of cats to empty their bladders completely. In anaesthetized cats, ganglion blocking agents prevented a rise in bladder pressure during sacral ventral root stimulation but a hyoscine-sensitive bladder contraction was seen following the period of stimulation. Further stimulation during this post-stimulus rise in intravesical pressure revealed a hyoscine-sensitive stimulus-bound relaxation. Sacral ventral root stimulation relaxed the bladder neck/proximal urethra particularly in the presence of sympathetic tone.

Incompetent urethral closure mechanism in females. Experimental and clinical studies with special reference to diagnosis and classification.

A urethral/bladder model was placed in a reservoir simulating the abdominal cavity. Increased "intraabdominal' pressure was transmitted to the urethra-like part of the model only when this was situated inside the "abdominal cavity'. The use of H2O and CO2 as filling medium was indifferent as only the relation between rise in urethral pressure and in bladder pressure is of practical importance. However, the increase in transmitted pressure was 25% lower than CO2 was used. Incompetent urethral closure mechanism is found in three categories of female patients: (1) patients with sensory urge who have an unstable urethra, (2) patients with genuine stress incontinence, and (3) patients who have a sphincteric insufficiency due to a low maximal urethral closure pressure and atrophy of the urethral mucosa. These categories can be separated urodynamically using simultaneous urethracystometry combined with transmission studies. Out of 20 patients with sensory urge 16 were found to have an unstable urethra. Transmission studies in 51 women with symptoms of stress incontinence revealed positive transmission, i.e. the increase in urethral pressure exceeded the rise in bladder pressure, in 23 patients. They were all elderly women and had a low maximal urethral closure pressure and their leakage of urine was due to an endourethral weakness. The remaining 28 patients had negative transmission and thus genuine stress incontinence. To classify the three different types of incompetent urethral closure mechanism it is necessary to perform a simultaneous urethracystometry, in which transmission studies are mandatory, as this is the most appropriate way to distinguish between patients who will benefit from operation and patients who will not.

Urethrocystometric findings in urgency.

15 women with chronic urgency have been examined with simultaneous urethrocystometry during an exacerbation of their disease. A thin microtip transducer catheter was used for pressure registrations. Both the bladder pressure and the maximal urethral pressure in the erect position were recorded during slow filling of the bladder. Although the patients had severe symptoms of frequency and in some cases urge incontinence in daily life, bladder capacity was almost normal. The desire to void appeared early but was not accompanied by a rise in bladder pressure. Even when the patients felt violent tenesmi, the bladder pressure curve remained completely calm. Only the urethral pressure reacted, with rapid rises and falls of 20--40 mm Hg, as the patients desperately tried to hold urine. Thus, no detrusor activity, but only a certain instability of the urethral pressure accompanied the subjectively imperious desire to void in urgency.

Neurophysiological aspects of enuresis.

The effects on the bladder motility of ablation and stimulation of certain peripheral and central nervous structures in the cat are summarized. It appears that the bladder emptying is controlled by two reflex mechanisms, viz., a spinal adaptation reflex with the effect of counteracting the rise in bladder pressure on filling, and the pontine micturition reflex. The excitability of the latter is influenced by more rostrally situated areas. By lesioning the medial and lateral parts of the amygdala nuclei complex it was found that the medial part inhibits and the lateral part facilitates micturition. From previous works it is known that the same parts of the complex respectively increase and decrease the reflex threshold of striated muscles, and that the medial part is necessary for defence and passive avoidance behaviour, while the lateral is necessary for flight and active avoidance behaviour. Based on the experimental results, the possible etiology of enuresis, the relationship between this disorder and epilepsy, as well as emotional changes claimed to occur in enuretic patients, are discussed.

Nervous control of urinary bladder in cats. I. The collecting phase.

AbstractEdvardsen, P. Nervous control of urinary bladder in cats. I. The collecting phase. Acta physiol. scand. 1968. 72. 157–171.Intravesical pressure under isometric conditions was studied in anesthetized cats after operative canalization of the bladder. Records were obtained after selective transection at the peripheral and at the intraspinal level of the sympathetic and parasympathetic nerves supplying the bladder, after rhizotomy of the thoraco‐lumbar and sacral nerves to the bladder, and after transection of the spinal cord at various levels. With small bladder volumes no change in pressure was observed after the various lesions, but as the volume increased, the concomitant rise in bladder pressure was progressively inhibited by sympathetic nervous impulses. In particular was this inhibition marked during the last one‐third of the cystometrogram. The sympathetic influefice is maintained by a spinal ieflex with the afferent path through the posterior sacral roots, its stimulus being stretching of the bladder wall. The effect of this spinal adaptation reflex is thus to permit increasing bladder volumes with only moderate increases in bladder pressure. ‘Nonspecific’ bladder responses consisted in an increase in motility caused by the laparotomy, and an inhibition of motility caused by any intraspinal procedure. This inhibitory effect was found to be due to discharge through the sympathetic nerves on manipulation of spinal structures, regardless of their relation to the segments supplying the bladder.

Nervous Control of Urinary Bladder in Cats

AbstractIntravesical pressure under isometric conditions was studied in anesthetized cats after operative canalization of the bladder. Records were obtained after selective transection at the peripheral and at the intraspinal level of the sympathetic and parasympathetic nerves supplying the bladder, after rhizotomy of the thoraco‐lumbar and sacral nerves to the bladder, and after transection of the spinal cord at various levels. With small bladder volumes no change in pressure was observed after the various lesions, but as the volume increased, the concomitant rise in bladder pressure was progressively inhibited by sympathetic nervous impulses. In particular was this inhibition marked during the last one‐third of the cystometrogram. The sympathetic influence is maintained by a spinal reflex with the afferent path through the posterior sacral roots, its stimulus being stretching of the bladder wall. The effect of this spinal adaptation reflex is thus to permit increasing bladder volumes with only moderate increases in bladder pressure. ‘Nonspecific’ bladder responses consisted in an increase in motility caused by the laparotomy, and an inhibition of motility caused by any intraspinal procedure. This inhibitory effect was found to be due to discharge through the sympathetic nerves on manipulation of spinal structures, regardless of their relation to the segments supplying the bladder.

Nervous control of urinary bladder in cats. A survey of recent experimental results and their relation to clinical problems.

Intravesical pressure under isometric conditions was studied in anesthetized cats after operative canalization of the bladder. Records were obtained after selective transection at the peripheral and at the intraspinal level of the sympathetic and parasympathetic nerves supplying the bladder, after rhizotomy of the thoraco-lumbar and sacral nerves to the bladder, and after transection of the spinal cord at various levels. With small bladder volumes no change in pressure was observed after the various lesions, but as the volume increased, the concomitant rise in bladder pressure was progressively inhibited by sympathetic nervous impulses. In particular was this inhibition marked during the last one-third of the cystometrogram. The sympathetic influence is maintained by a spinal reflex with the afferent path through the posterior sacral roots, its stimulus being stretching of the bladder wall. The effect of this spinal adaptation reflex is thus to permit increasing bladder volumes with only moderate increases in bladder pressure. ‘Nonspecific’ bladder responses consisted in an increase in motility caused by the laparotomy, and an inhibition of motility caused by any intraspinal procedure. This inhibitory effect was found to be due to discharge through the sympathetic nerves on manipulation of spinal structures, regardless of their relation to the segments supplying the bladder.