Resting Bladder Pressure Research Articles

Effects of anesthetics on cystometric parameters in female rats

The purpose of this study was to evaluate the effect of ketamine, propofol, midazolam and ether on cystometric parameters in rats. Thirty adult female Wistar rats were divided into four groups according to the agent used for the anesthesia; group 1: ether inhalation, group 2: midazolam, group 3: propofol and group 4: ketamine. After surgical implantation of catheter, cystometry was performed in awake rats followed by same procedure under anesthesia. Immediately following awake cystometry, six rats were anesthetized with midazolam (25 mg/kg) intraperitoneally (i.p.), seven rats were anesthetized with propofol (20 mg/kg) i.p., and 11 rats were anesthetized with ketamine (15 mg/kg) i.p. In other six rats, ether inhalation anesthesia was used after awake cystometry. Cystometric parameters such as resting bladder pressure, micturition pressure and the period between micturition were analyzed with Wilcoxon signed-rank test for statistical analysis. There was no statistically significant effect of ether and midazolam on cystometric parameters, compared to awake rats. Propofol was found to change all measured cystometric parameters without statistically significant difference. The period between micturition was clearly prolonged by propofol but it was also not statistically significant. Ketamine was found to be very depressant on micturition. The results suggest that ether and midazolam are preferable to ketamine for anesthetized cystometry studies. The results were questionable for propofol, and further studies are needed to make it clear.

Effect of Memantine on Overactive Detrusor in Rats With Spinal Cord Injury

The aim of this study was to determine the effect of memantine on overactive detrusor (OAD) 15 days after spinal cord injury (SCI) in rats. Twenty-eight adult Wistar rats were used in this study. Fourteen animals served as normal controls, while 14 underwent spinal cord transection (clip compression technique) at the 10th thoracic vertebra. Fifteen days after SCI, all animals underwent urodynamic testing to confirm OAD. Memantine (16 mg/kg) was injected intraperitoneally into rats with SCI and OAD. Parameters measured included voiding volume, micturition pressure, resting bladder pressure, the period between micturitions and the maximum pressure of the OAD during the filling period. Results have showed that OAD developed in 8/14 animals (57.1%). OAD was resolved in 5/8 (62.5%) of these animals after memantine administration. Resting bladder pressure was significantly different in dependent groups (p < 0.05). Micturition pressure increased after SCI but decreased in rats with SCI after memantine injection. However, the period between micturitions was prolonged in both SCI and memantine groups, compared with normal rats. These results show that memantine could be useful for treating neurogenic OAD after SCI by modulating the micturition reflex pathway. Memantine may also provide an alternative treatment option for OAD in the future.

Interstitial cells and phasic activity in the isolated mouse bladder

To describe the distribution of interstitial cells (ICs, defined as cells which show an increase in cGMP in response to nitric oxide, NO) in the isolated mouse bladder, and changes in phasic contractile activity after exposure to a NO donor. The whole bladder was removed from 17 female mice, killed by cervical dislocation. For immunohistochemistry (six mice) the bladder was incubated in carboxygenated Krebs' solution at 36 degrees C, containing 1 mm of the phosphodiesterase inhibitor isobutyl-methyl-xanthine. Individual pieces of tissue were exposed to 100 microm of the NO donor diethylamine NONOate for 10 min; control tissues remained in Krebs' solution. Tissues were then fixed in 4% paraformaldehyde and processed for cGMP immunohistochemistry. Bladder pressure was measured in bladders from 11 mice; the bladders were cannulated via the urethra and suspended in a heated chamber containing carboxygenated Tyrode solution at 33-35 degrees C and intravesical pressure recorded. All drugs were added to the solution bathing the abluminal surface. NO induced an increase in cGMP in cells in the outer layers of the bladder wall, forming two distinct types based on their location; cells lying on the surface of the muscle bundles (surface muscle ICs) and cells within the muscle bundles (intramuscular ICs). Cholinergic nerve fibres were identified by the expression of vesicular acetylcholine transporter and neuronal NO synthase (nNOS). Choline acetyltransferase- and nNOS-positive nerves also had high cGMP levels in response to 100 microm diethylamine NONOate. In vitro exposure of an isolated whole unstimulated bladder to 100 microm diethylamine NONOate had no effect on resting bladder pressure. When whole bladders were exposed to muscarinic stimulation (30-100 nm arecaidine) there was an initial large transient rise in pressure followed by complex phasic changes in pressure. Adding 100 microm diethylamine NONOate abolished this phasic activity. Interestingly, the phasic activity was inhibited midway between the peak and trough of a phasic cycle. Such a pattern of inhibition might reflect the complexity of the phasic activity involving both excitatory and inhibitory components. These data show the presence of NO/cGMP-sensitive ICs in the outer muscle layers of the mouse bladder. Activating these cells alters the pattern of muscarinic-induced phasic activity. We suggest that the role of the ICs in the outer muscle layers is to generate and modulate phasic activity. If so, then this is the first report of a functional role for ICs in the bladder.

Mechanisms of female urinary continence under stress: frequency spectrum analysis

Intravesical and urethral pressure signals during cough and Valsalva maneuvers for 15 continent women were analyzed with frequency spectrum analysis. Clear modulation of the urethral pressure changes by the intravesical pressure rise during stress maneuvers was demonstrated in the frequency bands of 14 and 7 Hz for cough and Valsalva, respectively. The linearity between the urethral and intravesical pressure signals was strong for cough, but relatively weaker for Valsalva. The observed linearity lead to the formulation of a modified continence equation to mathematically quantify stress leak point pressure (sLPP): sLPP=MUCP/(1− α1)+RBP. This algebraic equation demonstrated that sLPP depends on pressure transmission, resting bladder pressure, and maximum urethral closure pressure. The equation was validated with excellent theoretical predictions for the 15 continent subjects ( R 2=0.98 and 0.97 for cough and Valsalva leak point pressure, respectively) and good but somewhat weaker predictions for 46 stress incontinent women ( R 2=0.79 and 0.48, respectively). It has been shown that pressure transmission plays the most important role in female continence function, while it may be attributable to passive structural origin as evidenced by the minimal time delay between the two pressure signals, in the order of a few milliseconds. It can be concluded that coughing seems to have a more mechanical, rather than neuromuscular basis for its signal dynamics. This study suggests that a complete assessment of female stress continence function requires comprehensive urodynamic information in terms of pressure transmission, maximum urethral closure pressure, and resting bladder pressure.

The role of ATP-receptor in controlling the urinary bladder and urethral function in rats

The detrusor contraction involves an atropine resistant, nonadrenergic noncholinergic (NANC), component. Since adenosine triphosphate (ATP) has been proposed as a NANC transmitter, the role of ATP-receptors in the lower urinary tract was examined. The isovolumetric bladder contractions and the urethral pressure were monitored after intra-arterial administration of ATP analogues and other drugs in 52 female SD rats under intraperitoneal urethane anesthesia. alpha beta metATP induced a rapid, phasic increase of the maximal bladder pressure immediately after the drug administration, which was followed by a decrease during the P 2 X-purinoceptor desensitization period, but it did not affect the resting bladder pressure. RB-2 did not affect both the maximal bladder pressure and the resting bladder pressure. As for the urethral functions, alpha beta metATP induced a decrease of the resting urethral pressure during the P 2 X-purinoceptors desensitization period, while RB-2 induced a increase of the resting urethral pressure in contrast. ATP, alpha beta metATP and RB-2 did not changed the maximal urethral relaxation. The results will indicate that ATP produces detrusor contractions through the P 2 X-purinoceptor. Although ATP dose not affect urethral relaxation during voiding phase, it controls the urethral tone during collecting phase by both the excitation of P 2 X-purinoceptor and the inhibition of P 2 Y-purinoceptor.

Mechanisms of renal damage in chronic pyelonephritis (reflux nephropathy).

The relation between vesicoureteral reflux and pyelonephritis was first pointed out in a study of patients with neurogenic bladder (HUtch 1952). Almost 10 years later, studies done by HOdson and EDwards (1960) indicated the importance of intrarenal reflux in the pathogenesis of chronic pyelonephritis. Further studies by HOdson et al. (1975), using the pig as an experimental animal, showed that sterile reflux could produce renal scars in the areas of intrarenal reflux. His model, however, required bladder neck obstruction and a high voiding pressure in order to produce the high-grade reflux. While Hodson felt that sterile reflux damages the kidney, RANSLEY and RISDON’S study (1978) in the same model did not confirm Hodson’s work, and they showed that scarring from sterile reflux would occur only if the bladder neck obstruction was severe enough to cause high-pressure reflux. This has been confirmed in another pig model of obstructive reflux (JOrgeson 1986). We also confirmed these latter studies in the monkey, showing that after bladder neck obstruction, increased voiding and resting bladder pressure as well as peristaltic failure of the ureter led to transmission of these high pressures to the kidney with renal damage and interstitial nephritis (MEndoza and ROberts 1983). Neurogenic sphincteric dysfunction such as that which occurs in myelodysplasia may also cause high-pressure voiding, which will cause renal damage whether reflux is present or not, as shown in studies of myelodysplastic patients (MCGUIRE et al. 1981). The studies of Allen (1977), HInman (1973), KOff and MUrtagh (1984), and VAn Gool (1979) all showed that the dysfunctional voiding which can occur in neurologically normal children, may cause not only reflux, but also renal damage from voiding pressures as high as 150 cm of water.

Chronic retention of urine. The relationship between upper tract dilatation and bladder pressure.

Twenty-five men with chronic retention of urine were studied in order to investigate the relationship between upper tract dilatation and bladder pressure. Each underwent assessment of upper tract dilatation and urodynamic investigation before bladder drainage. Patients were reassessed 3 or more months after operation. Residual urine and detrusor contraction pressure decreased significantly after operation (P less than 0.0001:P less than 0.01). A significant increase in effective cystometric capacity and a significant decrease in pressure rise during filling led to an improvement in compliance. At pre-operative assessment, patients with upper tract dilatation had a significantly greater resting bladder pressure (P less than 0.05), end filling pressure (P less than 0.002) and pressure rise during filling (P less than 0.02) than those without upper tract dilatation. In addition, statistically significant correlations were found between serum creatinine and end filling pressure (P less than 0.05) and between upper tract dilatation and both high end filling pressure (greater than 25 cm H2O) and high pressure rise during filling (greater than 15 cm H2O: both P less than 0.05). Whilst high end filling pressure and high pressure rise during filling were found to be closely associated with upper tract dilatation (sensitivity 93 and 100%), there was a high false positive rate (specificity 64 and 45%). Furthermore, statistical analysis demonstrated that these data had a continuous though skewed distribution, suggesting that it is not possible to make a clear distinction between high and low pressure chronic retention.

5-Microtransducer catheter in evaluation of neurogenic bladder function

Recent use of the multiple microtransducer catheter in the evaluation of neurogenic bladder due to spinal-cord injuries leads us to believe that (1) the use of the inferior edge of the symphysis pubis as the zero point for resting bladder pressure is more accurate than its superior edge, (2) changes in resting bladder pressure at various volumes are influenced more by body position than by intravesical position of the sensor, (3) back-to-back microtransducers indicate significant pressure difference at the external sphincter zone, and (4) detrusor bladder neck dyssynergia during autonomic dysreflexia in patients with spinal cord injury is more likely of skeletal than of smooth muscle origin.

Renal pelvic pressures in human chronic obstructive uropathy.

Resting renal pelvic pressure and premicturition bladder pressure have been measured by direct percutaneous puncture in 12 male patients with established chronic obstructive uropathy related to high pressure chronic retention. In 10 technically satisfactory cases the subtracted renal pelvic pressure was less than the intrinsic bladder pressure, showing that upper tract dilatation and diminished renal function in these patients were not due to direct extension of high resting bladder pressure into the upper tract. The mean resting upper tract pressure in chronic human obstructive uropathy was 10.7 cm of water.

Effects of Sterile High Pressure Vesicoureteral Reflux on the Monkey

We surgically produced high-grade sterile vesicoureteral reflux in infant monkeys by unroofing the intravesical ureter and partially ligating the bladder neck. Half of the monkeys developed a decrease in renal function and were found to have interstitial nephritis. We found that this was due to a high resting bladder pressure, which affected the function and structure of the ureter. Thus, when a functional obstruction occurs in the refluxing ureter, renal function may be lost even when the urine is sterile. This situation is like that occurring in the patient with posterior urethral valves.

Effect of posture on bladder and urethral function in normal pregnancy. A preliminary report.

25 pregnant women, 15 of whom developed stress incontinence in pregnancy, have been investigated by cystometry and urethrometry in both erect and supine posture. The resting bladder pressure rises throughout pregnancy in both erect and supine positions. Those who are not incontinent have normal bladder and urethral function. Incontinent patients show no residual urine, normal bladder capacity, and either detrusor instability and/or sphincter weakness. The stress of change of posture makes both bladder dysfunction and sphincter weakness more evident. Although the results of this investigation are not yet complete, there is a suggestion that detrusor instability may be produced by pregnancy in some patients and that in some instances recovery to normal bladder function occurs after delivery. It is postulated that these patients may be the ones who, in later life, develop stress incontinence due to bladder dysfunction.