Increase In Bladder Pressure Research Articles

実験的糖尿病ラットの下部尿路機能に関する研究

Diabetic lower urinary tract disfunction is well known, however, precise mechanism of the lower urinary tract disfunction remains to be solved. The present study is to clarify the lower urinary tract disfunction of diabetic rats by simultaneously measuring bladder and urethral pressures. Female wistar rats were administered with streptozotocin (STZ 65 mg/kg, i.p.) to induce diabetes mellitus. Bladder and urethral pressures during rhythmic bladder contractions were compared under urethane anesthesia (1.0 g/kg, i.v.) between the control rats, diabetic rats, and diuretic rats. The bladder contraction pressures of diabetic rats were decreased initially, but returned to the control values at 8 weeks. Atropine (2.5 mg/kg, i.a.) produced a marked reduction of bladder contraction pressure in the 8 weeks diabetic rats. The diabetic rats showed an increase of urethral pressure simultaneously with an increase of bladder pressure in the initial phase of rhythmic bladder contraction which is totally blocked by striated muscle relaxant. This phenomenon was not observed in the control or diuretic rats. Both group showed an initial decrease of urethral pressure followed by bladder contraction and rhythmic contractions of the urethra. Our results suggest that bladder muscarinic receptors of the 8 weeks diabetic rats are more dominant than those of the other groups, and Mahoney's 4th reflex (urethrosphincteric guarding reflex) is facilitated but Mahoney's 6th reflex (detruthodetrusor facilitative reflex) is suppressed in the diabetic rats. We think that in the diabetic rats, sensory inputs by bladder distension were weak and could not induce Mahoney's 6th reflex until certain threshold values. Diabetic rats might develop changes in the mode of spinal neuronal transmission.

Vesicoureteral reflux in children

The association between vesicoureteral reflux and urinary tract infection represents a significant threat to the kidney, in the form of pyelonephritic scarring. The physiopathologic events that allow the upward migration of bacteria and their inoculation in the renal tissue, causing irreversible damage if not adequately treated, are reasonably understood. Reflux nephropathy is a major cause of childhood hypertension and renal insufficiency. Early diagnosis of reflux, and identification of the pyelonephritic aggression are important for successful therapy. Long-term chemoprophylaxis,to prevent urinary tract infection and renal scarring is the adequate form of treating low-grade vesicoureteric reflux, since spontaneous cure is expected in most of these cases. Although the same approach can be employed in high-grade reflux, surgery is a favorable alternative, with high rates of primary success,reducing the need of long-term medication and the exposure of the kidney to recurring pyelonephritic aggression. The retrograde flow of urine from the bladder to the upper urinary tract is an abnormal situation in the human being, known as vesicoureteral reflux (VUR). It results either from an intrinsic anatomical deficiency of the vesicoureteral junction or from an increased bladder pressure, due to mechanical or dysfunctional vesicourethral obstruction. The recognition of the association between VUR, urinary tract infection (UTI) and renal scars has led to an increased study of this disease in the last two decades.

Prostaglandin E sub 2 −Induced Bladder Hyperactivity in Normal, Conscious Rats: Involvement of Tachykinins?

In normal conscious rats investigated by continuous cystometry, intravesically instilled prostaglandin (PG) E sub 2 facilitated micturition and increased basal intravesical pressure. The effect was attenuated by both the NK 1 receptor selective antagonist RP 67,580 and the NK 2 receptor selective antagonist SR 48,968, given intra-arterially, suggesting that it was mediated by stimulation of both NK 1 and NK 2 receptors. Intra-arterially given PGE 2 produced a distinct increase in bladder pressure before initiating a micturition reflex, indicating that the PG had a direct contractant effect on the detrusor smooth muscle. The effect of intra-arterial PGE 2 could not be blocked by intra-arterial RP 67,580 or SR 48,968, which opens the possibility that the micturition reflex elicited by intra-arterial PGE 2 was mediated by pathways other than the reflex initiated when the PG was given intravesically. The present results thus suggest that intra-arterial PGE 2, given near the bladder, may initiate micturition in the normal rat chiefly by directly contracting the smooth muscle of the detrusor. However, when given intravesically, PGE 2 may stimulate micturition by releasing tachykinins from nerves in and/or immediately below the urothelium. These tachykinins, in turn, initiate a micturition reflex by stimulating NK 1 and NK 2 receptors. Prostanoids may, via release of tachykinins, contribute to both urge and bladder hyperactivity seen in inflammatory conditions of the lower urinary tract.

Contribution of alpha- and beta- adrenoceptors and neuropeptide-Y to autonomic dysreflexia.

Modest increases in urinary bladder pressure result in acute hypertensive episodes in humans with spinal cord lesions above T5. The underlying mechanisms of this condition, referred to as autonomic dysreflexia, are not well understood. The aim of this study was to characterize the contribution of alpha- and beta-adrenoceptors as well as circulating neuropeptide-Y (NPY) to the pressor response to bladder distension in conscious cervical spinal rats. Rats were chronically instrumented with arterial and venous catheters. After 2-3 days, a complete spinal transection (C7) was performed, and the urinary bladder was catheterized: 24 h later, mean arterial pressure (MAP) responses to 5 min bladder distensions (+40) were measured under control conditions and after administration of specific autonomic antagonists. To assess the contribution of alpha and beta adrenergic mechanisms the alpha antagonist prazosin (0.45 mg/kg i.v.) and beta antagonist, propranolol (4 mg/kg i.v.), were administered individually or together. Blood samples were taken before, during and after bladder distension for determination of plasma NPY by radioimmunoassay. The pressor response to bladder distension was approximately 30 mmHg under control conditions. The response was attenuated (-38%), but not abolished, by prazosin. A similar attenuation (-41%) was observed with propranolol. There were no changes in plasma NPY in response to bladder distension. Finally, the pressor response was completely abolished by combined alpha- and beta-adrenergic blockade. These results suggest that autonomic dysreflexia is mediated exclusively by adrenergic receptors in the spinal rat. Moreover, both alpha and beta adrenergic receptors contribute to the pressor response induced by bladder distension in the conscious cervical spinal rat.

Pelvic and pudendal reflexes in the in vitro neonatal rat preparation

Pudendal-to-pelvic and pudendal-to-pudendal reflexes are described in an in vitro brainstem-spinal cord neonatal rat preparation. Cytometrograms and peripheral pelvic nerve recordings were used to monitor excitatory micturition reflexes evoked by tactile perineal stimulation or by continuous electrical stimulation of the sensory pudendal nerve. Micturition was characterized by an increased bladder pressure and a period of tonic pelvic nerve activity during which time fluid was expelled from the urethra. Single stimuli delivered to the sensory pudendal nerve evoked a phasic response in the pelvic nerve (pudendal-to-pelvic reflex) or pudendal motor nerve (pudendal-to-pudendal reflexes). The pudendal-to-pelvic reflex consisted of a single response occurring after a mean latency of 98 ± 24 ms. The pudendal-to-pudendal reflex was comprised of two responses, the first occurred at a mean latency of 105 ± 11 ms and the second at 383 ± 36 ms. Cervical or lower thoracic spinal transection did not alter the pudendal-to-pelvic reflex, however, the second component of the pudendal-to-pudendal reflex was abolished. The use of preganglionic pelvic and pudendal peripheral nerve recordings described in this study provide a direct measure of the reflex outflow from the CNS and can be used to examine developmental changes and neurochemical substrates within the CNS which contribute to micturition and coital reflexes in the rat.

Cigarette smoking and pure genuine stress incontinence of urine: A comparison of risk factors and determinants between smokers and nonsmokers

OBJECTIVES: The aim of this case-control study was to examine differences in risk factors and determinants of genuine stress incontinence between smokers and nonsmokers. STUDY DESIGN: Seventy one smokers and 118 nonsmokers with pure genuine stress incontinence underwent a complete urogynecologic evaluation. Differences in risk factors and determinants of genuine stress incontinence were analyzed by means of χ2 and nonparametric techniques. RESULTS: Smokers had stronger urethral sphincters and generated greater increases in bladder pressure with coughing but had equivalent urethral mobility and pressure transmission ratios compared with nonsmokers. Smokers were significantly younger than nonsmokers, tended to be less often hypoestrogenic, but were of equivalent vaginal parity and weight. CONCLUSIONS: Genuine stress incontinence develops in smokers in spite of their stronger urethral sphincter and lower risk profile than nonsmokers. More violent coughing by smokers likely promotes the earlier development of the anatomic and pressure transmission defects that allow genuine stress incontinence and overcomes any protective advantage of a stronger urethral sphincter. (AM J OBSTET GYNECOL 1994;170:579-82.)

Micturition and Premicturition Contractions in Unanesthetized Rats with Bladder Outlet Obstruction

The cholinergic and purinergic neurotransmission involved in micturition contraction and premicturition contractile activity (bladder hyperactivity) were investigated by continuous cystometry in unanesthetized rats with outlet obstruction. Adenosine triphosphate (ATP), administered intraarterially close to the bladder, produced rapid, phasic dose-dependent increases in bladder pressure and micturition immediately after the injections. The percentage volume expelled was 74 ± 9% after 5 mg./kg. Intra-arterial α,β-methylene ATP also produced a rapid, phasic increase in bladder pressure and micturition immediately after the injection. The percentage volume expelled was 96 ± 3% after 1 mg./kg.; the residual volume of the following voidings increased, and the micturition pressure tended to decrease. However, dribbling incontinence was not produced. The amplitude of the premicturition contractions decreased significantly (p <0.01) after the administration. Intraarterial carbachol produced rapid, longlasting dose-dependent increases in bladder pressure and micturition. The percentage volume expelled was 88 ± 4 after 5 Mg./kg. Bladder capacity and micturition volume decreased significantly (p <0.05) during the following spontaneous voidings. Intra-arterial atropine (1 mg./kg.) increased bladder capacity (p <0.01) and residual volume (p <0.01), and tended to decrease micturition pressure (by 25%) and micturition volume. However, micturition contractions still remained after the injection, even if they changed appearance, and were of shorter duration. Atropine had no effect on the premicturition contractions. In the presence of atropine, α,β-methylene ATP initially produced a rapid, phasic increase in bladder pressure with micturition. Then, dribbling incontinence was observed in 1 of 5 animals.Hexamethonium, administered intra-arterially in doses producing urinary retention and dribbling incontinence (20 or 40 mg./kg.), increased the amplitude of the premicturition contractions, but decreased the frequency of the contractions. Intra-arterial tetrodotoxin (15 μg./kg.) inhibited micturition, and produced dribbling incontinence in all animals tested (n = 6). However, the amplitude of the premicturition contractions was not suppressed. Intra-arterial (±)-pinacidil (0.2 mg./kg.) significantly (p <0.05) decreased both amplitude and frequency of these contractions.It is concluded that both cholinergic and purinergic transmission seem to be of importance for pressure generation and emptying of the bladder in rats with outlet obstruction. The present results also give further support for the view that the premicturition contractions seen in these animals are of myogenic origin.

Functional importance of cholinergic and purinergic neurotransmission for micturition contraction in the normal, unanaesthetized rat.

1. The cholinergic and purinergic neurotransmission involved in micturition in the normal, unanaesthetized rat was investigated by means of continuous cystometry. 2. ATP (1 and 5 mg kg-1), administered intra-arterially (i.a.) close to the bladder, produced rapid, phasic, dose-dependent increases in bladder pressure with micturition immediately after injection. The micturition pressure of the following spontaneous voidings increased, and bladder capacity, micturition volume, and residual volume decreased. Pretreatment with alpha,beta-methylene ATP (1 mg kg-1, i.a.) blocked the effects of ATP (5 mg kg-1). 3. alpha,beta-Methylene ATP (0.25, 0.5 and 1 mg kg-1, i.a.) produced rapid, phasic, increases in bladder pressure with micturition immediately after injection. The effects of alpha,beta-methylene ATP (0.25 mg kg-1, i.a.) were not affected by pretreatment with indomethacin (0.5-2 mg kg-1, i.a.). The micturition pressure of the subsequent spontaneous voidings decreased, and bladder capacity and residual volume increased. 4. Carbachol (5-50 micrograms kg-1, i.a.) produced rapid, sustained, dose-dependent increases in bladder pressure with micturition, and then increased basal pressure, threshold pressure, and micturition pressure, and decreased bladder capacity and micturition volume during the following spontaneous voidings. 5. Atropine (1 mg kg-1, i.a.) decreased micturition pressure and micturition volume, but did not induce dribbling incontinence. Micturition contractions still occurred after the injection, but changed in appearance and were of shorter duration than before. In the presence of atropine (1 mg kg-1, i.a.), alpha,beta-methylene ATP (1 mg kg-1, i.a.) produced initially a phasic increase in bladder pressure with micturition and then dribbling incontinence in all animals tested. 6. After blockade of the micturition reflex with morphine (10 microg intrathecally), ATP (5 mg kg-1, i.a.),alpha,beta-methylene ATP (0.25-1 mg kg-1 , i.a.), and carbachol (5-500 microg kg-1, i.a.) were unable to empty the bladder.7. The results suggest that drug-induced bladder emptying in the normal, unanaesthetized rat requires an intact micturition reflex and they support the view that the two physiologically important transmitters involved in micturition are acetylcholine and ATP.

Bladder distention activates noradrenergic locus coeruleus neurons by an excitatory amino acid mechanism

The present study was designed to determine the neurotransmitter(s) involved in activation of noradrenergic locus coeruleus neurons by urinary bladder distention. The spontaneous discharge rate of single locus coeruleus neurons was recorded from halothane-anesthetized rats during the physiological challenge of bladder distention. Intrabladder saline infusion (0.5 ml) increased bladder pressure by 77 ± 9.7mmHg ( n = 19) and this was associated with an increase in locus coeruleus discharge rate of 53 ± 4.8% ( n = 29). Simultaneous recordings of cortical electroencephalographic activity demonstrated that electroencephalographic activation, characterized by a decreased amplitude and tendency to shift from low frequency activity to higher frequency activity, was also associated with bladder distention. The role of corticotropin-releasing factor and excitatory amino acid inputs to the locus coeruleus in activation by bladder distention was tested in rats pretreated with a corticotropin-releasing factor antagonist, or excitatory amino acid antagonists. Intracerebroventricular administration of the corticotropin-releasing factor antagonist did not alter locus coeruleus activation by bladder distention. In contrast, both locus coeruleus activation and electroencephalographic activation associated with bladder distention were prevented by intracerebroventricular administration of kynurenic acid. The same dose of kynurenic acid also prevented locus coeruleus activation by repeated sciatic nerve stimulation, as previously reported. Local administration of kynurenic acid into the locus coeruleus greatly attenuated, but did not completely prevent the increase in locus coeruleus discharge elicited by bladder distention. Finally, locus coeruleus activation by bladder distention appeared to be mediated by excitatory amino acid receptors of the non- N-methyl- d-aspartate subtype because this was prevented by 6-cyano-7-nitroquinoxaline-2,3-dione, but not by 2-amino-5-phosphono-pentanoic acid. Taken together, these results implicate excitatory amino acid neurotransmission in locus coeruleus activation by bladder distention, and argue against a role for corticotropin-releasing factor. Additionally, these findings suggest that locus coeruleus activation may be important in arousal associated with bladder distention.

Ambulatory Monitoring of Bladder Pressure in Low Compliance Neurogenic Bladder Dysfunction

Upper tract dilatation is an important complication of neurogenic bladder dysfunction. Risk factors include incomplete bladder emptying with large residual volumes of urine and high tonic increases in bladder pressures during artificial filling. However, on natural bladder filling many of these patients do not have high tonic increases in detrusor pressures. We compared conventional urodynamic studies with ambulatory monitoring during natural bladder filling in 66 patients with low compliance neurogenic bladder dysfunction.There were marked differences in the tonic increase in bladder pressure during filling and in compliance during artificial bladder filling compared with ambulatory monitoring. Faster filling rates during artificial filling resulted in greater end filling pressures and lower compliance but the lowest increases in bladder pressure were found during ambulatory monitoring with natural bladder filling. During natural bladder filling significantly more patients had phasic changes in detrusor pressure; a high intensity of phasic activity during ambulatory monitoring correlated with high end filling pressures during artificial bladder filling. Upper tract dilatation was associated with large volumes of residual urine, high resting bladder pressures and low bladder compliance on filling at 100ml. per minute. However, upper tract dilatation was most strongly associated with high intensity phasic pressure activity during natural bladder filling in combination with high residual urine volumes and high resting bladder pressures. On multivariate statistical analysis the intensity of phasic pressure activity during ambulatory monitoring was the best discriminator between patients with dilated and normal upper tracts.Our study has highlighted important differences in the results obtained by artificial filling cystometry and ambulatory monitoring during natural bladder filling. In particular, high increases in pressure did not occur during natural bladder filling, apparently being replaced by phasic activity. Within this group of patients who had the high risk factor of low bladder compliance measured during artificial bladder filling, a combination of greater residual urine volumes, greater resting pressures and greater phasic activity during natural bladder filling was found in patients with upper tract dilatation.

Role of sympathetic innervation in the feline continence process under natural filling conditions.

1. The effect of the sympathetic innervation on the bladder detrusor muscle was assessed in pentobarbitone-anesthetized cats by measuring the changes in bladder wall tension that occurred during sympathetic ganglion blockade after filling the bladder at a natural rate. 2. At a point 60% of the way through the continence process, systemic sympathetic blockade was produced by intravenous trimethaphan, and selective blockade of postganglionic hypogastric nerve activity was produced by application of trimethaphan to the exposed inferior mesenteric ganglia. The level of blockade was monitored with an in-continuity hypogastric nerve recording. 3. During both systemic and selective ganglion blockade, there was an increase in baseline transmural bladder pressure and a decrease in the amplitude of nonmicturating contractions. 4. Although there was no change in the mean level of transmural bladder pressure during either systemic or selective blockade, there was a significant increase in the mean level of bladder wall mechanoreceptor discharge, suggesting that before the blockade sympathoinhibitory effects were greater than sympathoexcitatory effects. 5. Measurement of bladder wall mechanoreceptor discharge before and during ganglion blockade revealed a net sympathoinhibitory influence on the level of bladder wall tension under natural filling conditions. These results confirm that the detrusor muscle of the feline bladder is under both sympathoinhibitory and sympathoexcitatory influences for a significant portion of the continence process.

The effect of alpha-2 agonists and antagonists on the upper urinary tract of the rat.

We examined the effect of the selective alpha-2 agonist dexmedetomidine and antagonist atipamizole on the upper urinary tract, renal pelvic pressure and ureteral peristalsis. Experiments were performed on twelve Sprague-Dawley female rats weighing 275-323 grams, with administration of urethane (1.2 micrograms/kg). Ventilatory support was provided through a tracheotomy. A continuous normal saline infusion was maintained through the left iliac vein at a rate of 2.5 ml/hr. Arterial pressure was measured at the left iliac artery, which was cannulated with a PE-100 tube connected to a pressure transducer. A mid-line incision was then made from the xyphoid to the symphysis to expose the left kidney, both ureters, and the bladder. The bladder was intubated and drained to avoid bladder pressure increase. Measurements of urine output rate were made from the right ureter and renal pelvic or ureteral pressure was measured using a nephrostomy placed into the pelvis. A ureterostomy was produced by introducing another catheter, into the upper segment of the left ureter for ureteral pressure measurements. The rats were divided into two groups as follows: 1) dexmedetomidine group (n = 6); injected intravenously with 2 micrograms/kg of dexmedetomidine dissolved in 0.5 ml saline. 2) atipamizole group (n = 6); injected intravenously with 2 micrograms/kg of atipamizole dissolved in 0.5 ml saline. Ureteral peristaltic frequency, baseline pressure, and contraction amplitude were compared before, after, and between the bolus injections of 2 micrograms/kg dexmedetomidine (n = 6) or 2 micrograms/kg atipamizole (n = 6) in 0.5 ml saline. The results showed that dexmedetomidine at 2 micrograms/kg produced a significant decrease in arterial pressure and an increase in urine output from 1.2 + 0.8 to 3.6 + 1.2 ml/min. There was no effect on the baseline pelvic pressure of 6.8 + 1.2 cmH2O or amplitude of the renal pelvic contractions: 3.5 + 0.6 cmH2O. The frequency of pelvic contractions was reduced from 0.37 + 0.03 to 0.27 + 0.02 Hz. Atipamizole at 2 micrograms/kg produced a significant reduction in urine flow rate of 1.1 + 0.8 to 0.6 + 0.2 ml/min. Atipamizole also showed no significant effects on baseline pelvic pressure or frequency, but increased the amplitude of pelvic contractions from control values of 3.0 + 0.9 to 3.4 + 0.9 cmH2O. Dexmedetomidine reduced both the baseline ureteral pressure of 8.5 + 2.4 and peristaltic contraction pressure of 11.5 + 2.3 cmH2O in 4/6 rats. Atipamizole reduced base-line ureteral pressure and increased peristaltic rate.(ABSTRACT TRUNCATED AT 400 WORDS)

Cough transmission pressure to the bladder and urethra among continent and incontinent elderly women

Although cough transmission pressures to the bladder and urethra are now being measured as part of the evaluation of an incontinent woman, there has not been a comprehensive study specifically focused among continent and incontinent non-institutionalized elderly women in order to understand the meaning of such measurements. To determine the characteristics and significance of the cough transmission pressures to the bladder and urethra, measurements were obtained from 69 continent and 100 incontinent elderly female respondents as part of an extensive urodynamic testing. Results showed that during coughing in the standing position, the increase in bladder pressure is significantly stronger among stress incontinent respondents than among continent and non-stress incontinent respondents (p = 0.0022). The increase in urethral pressure in the same group is marginally significant (p = 0.066). The mean transmission pressure ratio (urethral pressure ÷ bladder pressure) is less than 100% in all groups. They were higher among continent respondents (90%) and non-stress incontinent respondents (97%) than stress incontinent respondents (83%); however, the mean values between the 3 groups were not significantly different. The mean cough transmission pressures were significantly higher among chronic coughers than non-chronic coughers. When controlled for chronic coughing, the stress incontinent respondents have a significantly higher bladder pressure than continent and non-stress incontinent respondents. Significance of these findings in relation to the mechanisms of female geriatric incontinence are presented.

Factors affecting swim bladder volume in rainbow trout (Oncorhynchus mykiss) held in gas supersaturated water

We examined the response of the rainbow trout (Oncorhynchus mykiss) swim bladder to gas supersaturated water. Cannulas positioned in the swim bladder of fish were connected to a pressure transducer, allowing direct measurement of swim bladder pressure. When denied access to the surface, fish held in supersaurated water showed an increase in swim bladder pressure. This response showed a strong dependence on the total gas pressure and the oxygen partial pressure of the water. The minimum level of gas supersaturation observed to cause this response corresponds to a ΔP of 27 mmHg [Formula: see text]; 1 mmHg = 133.3 Pa). The threshold ΔP for swim bladder inflation increased as the partial pressure of dissolved oxygen increased. Movement of supersaturated gases from the arterial system into the swim bladder is passive and causes a rise in swim bladder pressure until the diffusion gradient is nil or the gas is expelled through the pneumatic duct. The threshold for release of gas out the pneumatic duct is dependent on the size of the fish. Small fish have higher duct release pressures and are subject to a higher degree of pressure buildup within the swim bladder than larger fish.

Chronic cervical spinal cord injury and autonomic hyperreflexia in rats

Although it is well established that patients with cervical spinal cord injury are prone to acute, marked, hypertensive episodes, i.e., autonomic hyperreflexia, the specific mechanisms mediating this sometimes-fatal phenomenon are not completely understood. In this report, we describe the preparation and characterization of a rat model of chronic cervical spinal cord injury and autonomic hyperreflexia. Adult male Sprague-Dawley rats were chronically instrumented with arterial, venous, and gastric catheters. Beginning the first day after a complete cervical spinal transection (CST) and continuing for 1 wk, acute hypertensive responses to a modest increase of urinary bladder pressure (0-20 mmHg) were studied. Mean arterial pressure increased 25.9 +/- 4.8 mmHg during bladder distension the first day after CST. This response was not significantly different 3, 5, and 7 days after CST (overall average = 18.0 +/- 2.3 mmHg). The pressor response to bladder distension was completely abolished by intravesical lidocaine and autonomic ganglionic blockade (atropine + hexamethonium). Responses to bladder distension were not observed after the administration of chloralose anesthesia. We conclude that after cervical spinal transection the rat exhibits autonomic hyperreflexia similar to that seen in humans with spinal injury. Furthermore, autonomic hyperreflexia is completely established within 24 h after CST in the rat. Finally, some spinal autonomic reflexes are suppressed by chloralose anesthesia in the rat.

Effects of selective cholinergic antagonists and alpha,beta-methylene ATP on guinea-pig urinary bladder contractions in vivo following pelvic nerve stimulation.

1. An in vivo preparation measuring functional detrusor muscle strength in terms of intravesical bladder pressure (Pves) following in situ pelvic nerve stimulation has been developed in urethane-anaesthetized guinea pigs. 2. The increase in bladder pressure following pelvic nerve stimulation was abolished by topical lidocaine or tetrodotoxin, suggesting a neurogenic origin for the in vivo contractile response. 3. Cholinergic antagonists (i.v.) decreased the amplitude of the peak pressure response by about 50% at both high (30 Hz) and low (5 Hz) stimulation rates, with a rank order of potency of atropine greater than propantheline greater than oxybutynin greater than hexahydrosiladifenidol greater than pirenzepine greater than methoctramine. 4. The P2 purine receptor antagonist, alpha,beta-methylene ATP (i.v.), antagonized pelvic nerve-stimulated bladder contractions differentially at 5 and 30 Hz. At low frequencies, alpha, beta-methylene ATP was both more potent (2.5-fold) and more efficacious (-77 compared to -55% delta) than at 30 Hz. Atropine and alpha,beta-methylene ATP together completely inhibited the contractile response. 5. Together, the findings indicate that in guinea pigs, urinary bladder contractions induced by pelvic nerve stimulation in vivo may be mediated by both muscarinic and purinergic receptors and that these bladder contractions may be mediated by the M2 beta subtype rather than by M1 or M2 alpha muscarinic receptors.

Urodynamics in enuretics II: A pressure/flow study

AbstractThis study dealt with urodynamics during sleep where enuresis was provoked by filling cystometries. Data were compared to the ones obtained in the same patients in urodynamics at awake state. Fifty‐six sleep cystometries resulted in 31 enuretic events and 25 arousals. Comparison of pressures revealed that enuresis was taking place during an increase in maximal bladder pressure of 20 cm H2O (P&lt;0.05) and a prolonged contraction time (P&lt;0.05). The configuration of the pressure tracing was otherwise completely similar to the ones obtained in awake state. Furthermore, these were similar to data available in the literature of normal children. It is hence concluded that enuretics are urodynamically normal and that the enuretic event is a coordinated micturition initiated at maximal bladder capacity with some indication of increased urethral resistance.

Active Antireflux Mechanism Induced by Micturition Experimental Study in Awake Sheep

The influence of increased bladder pressure on ureteral peristalsis is described in the literature. All experiments were done on anesthetized animals and vesical contractions were electrically induced. We present an experiment on awake sheep. The animals voided spontaneously while a recording of the peristaltic pressure of the lower ureter was recorded. A rise in the peristaltic pressure in both ureters was observed during micturition. We suggest that the rise in ureteral pressure participates in the antireflux mechanism.

Effects of Five Alpha-Blockers on the Hypogastric Nerve Stimulation of the Canine Lower Urinary Tract

Electrical stimulation of the hypogastric nerve increased both urethral and bladder pressures of anaesthetized male dogs, without affecting cardiovascular parameters. Intravenous injections of prazosin, phentolamine, thymoxamine, phenoxybenzamine and yohimbine inhibited the urethral pressure increase in a dose-dependent manner, but the increase in bladder pressure was not modified by these alpha-blockers.

Urodynamic responses to sacral stimulation in the chronic spinal dog

AbstractRecent reports have shown that electrical stimulation of the bladder wall or sacral nerves can be effective for bladder management in the spinal‐cord‐injured (SCI) patient. However, unacceptable bladder pressures and urethral resistances have been reported in many of these patients following such stimulation procedures. These problems were evaluated in this study using epidural electrodes in the sacral canal of the chronic spinal male dog. We found that bladder reflex activity is important for sacral stimulation to induce effective voiding. Voiding in response to stimulation was poor during the first week following spinal injury but improved during the next 2 weeks. A significant increase in bladder pressure in response to stimulation occurred during this period, but urethral resistance remained unchanged. Urethral resistance, the ratio of bladder pressure to voiding rate, was lower for poststimulus voiding than for voiding during continuous stimulation. Bladder compliance, measured via cystometry, was improved in one spinal dog during a period of sacral stimulation. However, an adverse trend toward increased bladder thickness was seen on postmortem examination. Overall, this minimally invasive method was encouraging and may be efficacious for bladder control in some SCI patients.