Urodynamics of the lower urinary tract

Summary The principles and techniques of uroflowmetry, cystometry, pressure-flow studies and urethral pressure profilometry are reviewed. The interpretation of urodynamic tests depends on the methodology used and whether the patients usual voiding symptoms during the examination. The more complicated urodynamic tests may require computer assistance both for data storage but also for test interpretation. One of the main challenge in future urodynamic is to transform these tests to clinical usable tools.     

Anatomy of the lower urinary tract

The lower urinary tract (LUT) comprises the bladder and urethra in females with the addition of the prostate in males. The function of the lower tract is the low-pressure non-volitional storage of urine it receives from the upper urinary tract followed by the voluntary expulsion of urine when socially acceptable. The LUT may be affected by functional disorders such as bladder overactivity and urinary incontinence or by obstructive disorders such as prostatic enlargement and stricture disease or alternatively by other pathologies such as carcinoma and lithiasis. A thorough knowledge and understanding of the relevant anatomy is essential in understanding the various pathophysiological mechanisms of LUT disorders and their appropriate management. We describe the anatomy of the male and female LUT between which considerable differences exist in structure and function, in addition to summarizing the histology, vasculature and neural innervation of the organs comprising the LUT.     

Scleroderma of lower urinary tract

A case of scleroderma involving the lower urinary tract is reported. To our knowledge, this is the first instance of a living patient with this condition.     

Endourology of lower urinary tract

Two methods for obtaining percutaneous access to the bladder are described. Depending on whether or not urethral access is available an endoscopic or fluoroscopic technique may be applied. We have successfully performed suprapubic percutaneous cystolitholapaxy, antegrade fulguration of posterior urethral valves, antegrade cystourethroscopy as an adjunct for urethroplasty, and internal drainage of a bulbar urethral abscess. Endourologic techniques may be readily applied to the lower urinary tract and may be specifically indicated in certain situations.     

alpha-Blockers improve chronic ischaemia of the lower urinary tract in patients with lower urinary tract symptoms

OBJECTIVE

To investigate whether a mechanism of action of α‐blockers on lower urinary tract symptoms (LUTS) involves improved perfusion of the LUT.

PATIENTS, SUBJECTS AND METHODS

The accuracy of perfusion measurements using transrectal colour Doppler ultrasound (TRCDUS) and colour pixel density (CPD) was initially confirmed in a porcine model. Following this confirmation, measurements were taken from four healthy male volunteers and 19 patients with LUTS. The urinary bladder was filled slowly (50 mL/min) with 0.2 m KCl, which resembles the osmolarity of concentrated urine, and evaluated by cystometry. In parallel, TRCDUS and measurement of the CPD of the LUT were performed. The patients with LUTS were then treated with daily α‐blocker (0.4 mg tamsulosin) for 5 weeks and urodynamic variables as well as perfusion were evaluated again.

RESULTS

In the healthy men, perfusion of the LUT increased considerably (157%) during filling of the bladder to a mean (sd ) maximum cystometric capacity (C_max) of 481 (28.9) mL. All the patients with LUTS had a reduced mean C_max during filling with KCl at 322.4 (58.5) mL. The mean CPD in the urinary bladder and the prostate were only increased by 58.4% during filling with KCl. After α‐blocker therapy the mean C_max during filling with KCl rose to 382.5 (42.9) mL; furthermore, perfusion of the LUT measured by CPD was significantly increased (132.8%).

CONCLUSIONS

The present data strongly suggest that LUTS are associated with chronic ischaemia of the prostate and urinary bladder. α‐blockers increase perfusion in the LUT and C_max. These results might explain the therapeutic effects of α‐blockers on LUTS.     

Neurotransmission and the lower urinary tract

The neurotransmitter activity in the lower urinary tract is very complex. This paper reviews the main substances, known today, their agonists, antagonists, metabolic pathways and their action and discusses the site of action of neuropharmacological substances. The existence of a non-adrenergic, non-cholinergic pathway, in parallel with the sympathetic adrenergic and the parasympathetic cholinergic pathways is thus clearly admitted.     

Estrogens and the lower urinary tract

The urogenital tract is sensitive to the effect of oestrogen and progesterone throughout adult life. Epidemiological studies have implicated oestrogen deficiency in the aetiology of lower urinary tract symptoms occurring following the menopause. Although to date the role of oestrogen replacement therapy in the management of postmenopausal urinary incontinence remains controversial its use in the management of women complaining of urogenital atrophy is now well established. This aim of this paper is to review the recent evidence regarding the urogenital effects of hormone therapy with a particular emphasis on the management of postmenopausal urinary incontinence, overactive bladder, recurrent lower urinary tract infections and urogenital atrophy. In addition to a review of the available evidence suggestions are also made regarding priorities for further research in the field.     

Genetics and the lower urinary tract

Many complex disorders have been found to have a heritable component, including lower urinary tract dysfunction. Twin studies have indicated that genetic contributions to urinary incontinence (UI) may be as important as environmental influences. Linkage to chromosome 9 has been demonstrated in families with pelvic organ prolapse and stress UI. An increasing number of incontinence specialists are studying subjects with lower urinary tract dysfunction using single nucleotide polymorphisms, linkage analyses of siblings, and large association studies. These findings have exciting implications for future prevention and treatment of UI. Neurourol. Urodynam. 29:609–611, 2010. © 2010 Wiley‐Liss, Inc.     

Congenital abnormalities of the lower urinary tract

Congenital anomalies of the lower urinary tract and genitalia (such as hypospadias) are common, but the group comprises some conditions which are rare (such as the exstrophy–epispadias sequence) and whose surgical treatment is challenging. The breadth of conditions encountered in routine and specialized paediatric urological practice is described.     

Computed tomography of the lower urinary tract

CT can be helpful in staging bladder and prostate cancer as described previously. The limitations are significant in certain aspects of staging. It is important for the future to compare state-of-the-art computed tomographic scanning with newer imaging modalities such as magnetic resonance imaging, which is currently being evaluated for staging these particular tumors.     

Phosphodiesterase activity of the lower urinary tract

Cyclic AMP is believed to mediate the physiologic response of beta-receptor stimulation in the lower urinary tract. A possible novel therapy for specific dysfunctions might be via pharmacologic modification of cyclic AMP through regulation of phosphodiesterase, the enzyme responsible for metabolizing cyclic AMP. The present study characterizes the phosphodiesterase activity present in various sections of the lower urinary tract and determines the effect of calmodulin and the potency of a series of phosphodiesterase inhibitors. The results can be summarized as follows: the phosphodiesterase activity of all smooth muscle sections of the lower urinary tract were similar. They showed nonlinear kinetics with Vmax between 1.0 and 2.4 nmol./mg. protein/minute and apparent Km's around 100 microM. The external sphincter (skeletal muscle) displayed linear kinetics with a Vmax of 0.2 nmol./mg. protein/minute and a Km of 9 microM. Of the drugs tested, papaverine was the most potent inhibitor and theophylline was one of the weakest inhibitors. These studies also indicate that the major form of cyclic AMP phosphodiesterase is not sensitive to calmodulin.