Scandinavian journal of urology and nephrology. Supplementum最新文献

The bladder wall becomes to ischaemic when intravesical pressure rises above capillary pressure. This will occur routinely in bladders with outflow obstruction. Experiments in vitro show that the detrusor normally uses anaerobic as well as aerobic metabolism. Anoxic conditions result in an initial reduction in contractility, but significant contractile ability persists. Substrate removal causes a slow progressive fall in contractility as glycogen stores deplete. Removal of substrate and oxygen causes rapid loss of contractile ability and permanently damages intrinsic nerves, although the detrusor recovers well. In vivo ischaemia in animal models results in bladder overactivity and the expression of apoptotic markers in intrinsic neurons in the bladder wall. In humans, bladders from patients with bladder instability show patchy denervation, suggesting that periodic ischaemia and neuronal death may predispose to overactivity.

The purpose with the present review was to characterise bladder function in healthy preterm and full-term infants from findings in studies using the four-hour voiding observation. Characteristics of the free voiding pattern were very similar in preterm and full-term infants. The frequency of voidings was once an hour, bladder volume inducing voiding varied, infants often woke up before voiding and the bladder was not completely emptied at every voiding. Furthermore, interrupted voidings interpreted as a detrusor-sphincter dyscoordination, were seen and were clearly an immature phenomenon since the frequency was high in the preterm infants and then decreased. Concluding these findings the voiding pattern seems to be immature early in life and there is distinct evidence for a connection to the CNS already in the preterm infant.

Objective: To describe normal natural fill urodynamics in young men during normal and increased fluid intake.

Material and methods: Thirty healthy males aged 21-32 years volunteered for an ambulatory urodynamic 24 h investigation with a suprapubic catheter. The recorded micturition data were: frequency (f), voided volume (VV), voiding time, maximal flow rate (Qmax) and time to Qmax. The number of sensed and not-sensed bladder contractions, duration and time in relation to voiding were also recorded. During the recording day subjects were randomized to normal (30 ml/kg body weight per day) or larger (60 ml/kg body weight per day) fluid intake.

Results: As expected there was a larger urine production and an increased voiding frequency in the fluid-loaded group (p<0.0001). The detrusor pressure (Pdet) Qmax was significantly higher in the fluid-loaded group (73 cmH2O, range 57-94) than in the normal fluid intake group (60 cmH2O, range 45-86) (p=0.003). No other urodynamic data differed significantly between the two groups. When comparing the ambulatory urodynamic data with previously obtained home flowmetry recordings from the same volunteers differences were only found in voiding frequency. The majority of participants had detrusor contractions, felt and unfelt, during the filling phase. Three types of detrusor activity during voiding phase could be described: type 1, with one micturition contraction, type 2, with several small contractions before micturition, and type 3, with large prolonged contractions leading to micturition.

Conclusions: Ambulatory urodynamics in normal young men showed a large interindividual variation. Bladder contractions during filling were frequently recorded, and premicturition contractions were consistently found. The data found in this study were similar to previous home flow recordings in the same group.

Contractile activation of detrusor smooth muscle is initiated by the release of transmitters from motor nerves. Acetylcholine is a ubiquitous transmitter, as also is adenosine triphosphate (ATP) in many animal bladders and in people from several patient groups with pathological bladder function. In recent years there has been progress in explaining several cellular mechanisms that link transmitter release to contraction and these will be considered. The lifetime of ATP in the neuromuscular junction is finite and broken down ultimately to adenosine, which can exert modulatory control of contractile activation. Adenosine depresses nerve-mediated contractions and two sites of action have been proposed: an action on the motor nerves via A receptors to depress further transmitter release and a less well-defined depressant effect on the detrusor muscle. The Ca2+ ions that activate the contractile proteins are derived from intracellular stores, which releases their content via IP receptor activation and Ca2+-induced Ca2+ release. Filling of the stores in the rest interval is mediated via transmembrane flux of Ca2+through Ca2+ channels. Activation of the channels is regulated by the level of the intracellular [Ca2+], via activation and inactivation of Ca2+-sensitive K channels. Thus, Ca2+ store filling is regulated by intracellular [Ca2+] via a negative feedback process. The presence and physiological function of spontaneous contractions in detrusor remain contentious and little is known about their origin. One possibility is that they originate from random Ca2+ sparks, i.e. localized transient increases of [Ca2+] that may eventually progress to generate a cellular Ca2+ transient. Observations by confocal microscopy have revealed the presence of such sparks, especially near the cell membrane, and thus provide a cellular basis for spontaneous contractions. Finally, the questions arises as to whether detrusor smooth muscle is a functional syncitium. The demonstration of small gap junctions by electron microscopy and the demonstration of the gap junction protein connexin45 indicate that the muscle mass may indeed be functionally connected. The implications regarding the spread of excitation are discussed.

A review was conducted of the current knowledge of fetal and postnatal development of autonomic bladder function in animals. Studies of fetal and neonatal bladder development have been done in many animal species. Development of normal bladder function requires coordination of a number of different systems and processes, and continues after birth during the early neonatal period. In many neonatal animals, micturition occurs only after stimulation of a perineal-to-bladder reflex triggered when the mother licks the perineal region, and bladder distension fails to stimulate micturition. Voiding resulting from the normal bladder-to-bladder spinobulbospinal reflex activated by bladder distension develops only slowly over the first few weeks of life as synaptic connections in the sacral parasympathetic nucleus mature. The neurogenic response of bladder strips from young neonates is more sensitive to inhibition by atropine than that of strips from older animals, suggesting that there are developmental changes in the contribution of non-adrenergic, non-cholinergic transmitters to the response of the bladder smooth muscle to intramural nerve stimulation. Release of acetylcholine from cholinergic nerves and the mechanisms required to transform muscarinic receptor stimulation into efficient bladder contraction and emptying are fully developed at birth, but contractile and relaxant responses to many other agonists, such as adenosine triphosphate and noradrenaline, are developmentally regulated. Changes in calcium influx and storage may be responsible for many of these changes. Fetal detrusor is exquisitely sensitive to nitric oxide. Electrical stimulation of precontracted fetal bladder strips causes relaxation, an effect that is not seen in adult tissues, and is decreased by inhibitors of the actions of nitric oxide. Development of bladder function occurs before the onset of puberty and therefore is not normally dependent on sex hormones. However, neonatal treatment with or depletion of sex hormones can modulate bladder function. In particular, alpha-adrenergic receptor-mediated contractile responses of bladder detrusor are increased by prepubertal castration, an effect that may result from increases in the density of alpha-adrenergic receptors and/or changes in alpha-adrenergic receptor subtype expression.

Objective: To check the long-term effect, in male patients, of treated and untreated bladder outlet obstruction (BOO) on detrusor contractility and to explore the relationship between ageing and detrusor underactivity (DUA).

Material and methods: Men investigated at the urodynamic department of Southmead Hospital in Bristol between 1972 and 1986 were traced and three groups were invited for repeat pressure-flow urodynamic studies (PFS). The first two groups included patients over 40 years old, with untreated or surgically treated BOO, and the third group had patients with DUA from all age groups.

Results: 196 patients (with a minimum 10 year gap from the first assessment) agreed to have repeat PFS. There was no statistically significant change in bladder contractility index (BCI) in patients with BOO treated by transurethral resection of the prostate (TURP) (mean difference in BCI was 0.01, 95% confidence interval -0.07 to 0.09, n=114). There was also no significant difference in BCI in untreated patients with BOO (p=0.10, n=53). The follow-up BCI was higher in untreated patients than in the surgically treated group. The BCI in patients with DUA did not change significantly after a minimum of 10 years' follow-up.

Conclusions: There is no evidence to suggest that detrusor contractility declines with long-term BOO. Relieving the obstruction surgically does not improve the contractility. This is important when considering and counselling for TURP. Underactive detrusors remain underactive, but do not get worse with time, which could indicate that this is not an ageing process per se and may even have a congenital basis.

Benign prostatic hyperplasia (BPH) is a disease that has its etiology in the abnormal growth of the adult human prostate gland that accompanies the aging process in men. The symptomatic presentation of this disease, however, is related largely to degenerative changes in the bladder that occur as a result of the increasing urethral resistance and partial bladder outlet obstruction (PBOO) caused by the growing prostate gland. BPH is characterized by bladder hypertrophy, significant decreases in urinary flow and compliance, presence of residual urine after voiding, voiding urgency and incontinence (). Obstructed bladder dysfunction secondary to BPH is a slow, progressive disease that is so strongly associated with human aging that it is an expected occurrence of the male aging process. Although the symptoms of BPH are usually not life threatening, they effect an extremely negative quality of life for men who suffer from them. However, many men delay seeking medical treatment for early BPH since bladder function can remain relatively normal as the hypertrophying bladder initially compensates for the progressive increase in urethral resistance caused by prostatic obstruction. The limited changes in micturition pressure and flow characteristics that occur during compensated function are not usually disabling enough to motivate seeking medical attention, which, often, is not sought until the symptoms become typical of advanced disease. Recent advances in detection methods enable identification of patients with significant BPH during compensation before the bladder becomes dysfunctional (decompensated). A more complete understanding of the disease processes that underlie the loss of bladder function associated with BPH might enable the development of treatments that better protect these early-stage BPH patients from the more debilitating aspects of the disease. This review updates the understanding of obstructive bladder dysfunction via the use of animal models.