[Importance of uroflowmetry in lower urinary tract symptoms diagnostics]. / Význam uroflowmetrie v diagnostice poruch dolních mocových cest.

OBJECTIVE: To summarize the current state of knowledge on the use of uroflowmetry in diagnosis of lower urinary tract dysfunction in women. DESIGN: Review article. SETTING: Department of Obstetrics and Gynecology, University Hospital Ostrava and Faculty of Medicine, Ostrava University. METHODS: Literature review. RESULTS AND CONCLUSION: Lower urinary tract dysfunction is associated with debilitating symptoms, which negatively affect the quality of life of a large number of patients, and represent a significant health problem. Inaccurate diagnosis leads to delayed therapy, which could cause disease progression and complications. It has been recently recognized that affected patients express a wide variety of clinical phenotypes. Advancements in diagnostic procedures may allow for individualized treatment and improved treatment outcomes. Diagnostic procedures recommended for patients with suspected lower urinary tract disease include directed medical history, urinalysis, voiding diary, as well as non-invasive and invasive urodynamic methods. Additional diagnostic tests may be used in select cases. Uroflowmetry is a basic urodynamic method used for screening. It represents a standard component used in the diagnostic process for patients with lower urinary tract symptoms. Sonouroflowmetry is a new method, which evaluates the urinary flow and lower urinary tract symptoms in a non-invasive manner by analysing the sound generated by a stream of urine striking the water surface in the toilet bowl.

Cocaine- and amphetamine-regulated transcript peptide (CARTp): distribution and function in rat urinary bladder.

We investigated the distribution of CARTp(55-102) in rat lower urinary tract and evaluated its effect on urinary bladder function in vitro. Immunohistochemistry and a vertical isolated tissue bath system were used. Neurons, clusters of nonneuronal endocrine cells, and nerve fibers stained positive for CARTp(55-102) in young adult rat urinary bladder. The CARTp-expressing neuronal elements were nitric oxide synthase (NOS)- and tyrosine hydroxylase (TH)-IR, whereas all nonneuronal CARTp-IR elements stained positively only for TH (100 %). In isolated bladder strips, CARTp significantly increased the amplitude of electric field stimulation (EFS)-induced detrusor contractions at stimulation frequencies ≤12.5 Hz (p ≤ 0.001) as well as amplitude and frequency of spontaneous phasic urinary bladder smooth muscle (UBSM) contractions (p ≤ 0.05). The responses to CARTp stimulation were dose-dependent and increased in the presence of the urothelium. To determine if the CARTp increase in nerve-mediated contractions may involve an action of CARTp on specific neural pathways, we blocked cholinergic, purinergic, and adrenergic pathways and determined CARTp actions on EFS-medicated contractions. CARTp enhancement of EFS-mediated contractions does not involve alteration in purinergic, adrenergic, or cholinergic pathways. The study demonstrates that CARTp(55-102) is highly expressed in rat urinary bladder. CARTp increased the amplitude of EFS-induced detrusor contractions as well as the amplitude and frequency of spontaneous phasic urinary bladder smooth muscle contractions. We conclude that CARTp may alter the release of compounds from the urothelium that leads to an enhancement of UBSM contractility/excitability.

Acute and chronic effects of oxyhemoglobin on voltage-dependent ion channels in cerebral arteries.

Voltage-dependent potassium (Kv) and calcium (VDCC) channels play an important role in the regulation of membrane potential and intracellular calcium concentration in cerebral artery myocytes. Recent evidence suggests VDCC activity is increased and Kv channel activity is decreased in cerebral arteries following subarachnoid hemorrhage (SAH), promoting enhanced constriction. We have examined the impact of the blood component oxyhemoglobin on Kv and VDCC function in small (100-200 microm) diameter cerebral arteries. Acute (10 min) exposure of oxyhemoglobin caused cerebral artery constriction and Kv current suppression that was abolished by tyrosine kinase inhibitors and a Kv channel blocker. Although short-term oxyhemoglobin application did not directly alter VDCC activity, five-day exposure to oxyhemoglobin was associated with enhanced expression of voltage-dependent calcium channels. This work suggests that acute and chronic effects of oxyhemoglobin act synergistically to promote membrane depolarization and increased VDCC activity in cerebral arteries. These actions of oxyhemoglobin may contribute to the development of cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

Changes in galanin immunoreactivity in rat micturition reflex pathways after cyclophosphamide-induced cystitis.

Alterations in the expression of the neuropeptide, galanin, were examined in micturition reflex pathways of rat after cyclophosphamide (CYP)-induced cystitis of variable duration: acute (4 h), intermediate (48 h), or chronic (10 days). In control animals, galanin expression was present in specific regions of the gray matter in the rostral lumbar and caudal lumbosacral spinal cord, including: (1) the dorsal commissure (DCM); (2) superficial dorsal horn; (3) the regions of the intermediolateral cell column (L1-L2) and the sacral parasympathetic nucleus (SPN, L6-S1); and (4) the lateral collateral pathway (LCP) in lumbosacral spinal segments. Densitometry analysis demonstrated significant decreases (P< or =0.01) in galanin immunoreactivity (IR) in these regions of the L1-S1 spinal cord after acute or intermediate CYP-induced cystitis. In contrast, increases (P< or =0.01) in galanin-IR were observed in the DCM, SPN, or LCP regions in the L6-S1 spinal segments in rats with chronic cystitis. No changes in the number of galanin-immunoreactive cells were observed in the L1-S1 dorsal root ganglia (DRG) after CYP-induced cystitis of any duration. A small percentage of bladder afferent cells (Fast-blue-labeled) in the DRG expressed galanin-IR in control rats; this was not altered with cystitis. Galanin-IR was observed encircling DRG cells after chronic cystitis. These changes may contribute to urinary bladder dysfunction, altered sensation, and referred somatic hyperalgesia after cystitis.

Changes in galanin immunoreactivity in rat lumbosacral spinal cord and dorsal root ganglia after spinal cord injury.

Alterations in the expression of the neuropeptide galanin were examined in micturition reflex pathways 6 weeks after complete spinal cord transection (T8). In control animals, galanin expression was present in specific regions of the gray matter in the rostral lumbar and caudal lumbosacral spinal cord, including: (1) the dorsal commissure; (2) the superficial dorsal horn; (3) the regions of the intermediolateral cell column (L1-L2) and the sacral parasympathetic nucleus (L6-S1); and (4) the lateral collateral pathway in lumbosacral spinal segments. Densitometry analysis demonstrated significant increases (P < or = 0.001) in galanin immunoreactivity (IR) in these regions of the S1 spinal cord after spinal cord injury (SCI). Changes in galanin-IR were not observed at the L4-L6 segments except for an increase in galanin-IR in the dorsal commissure in the L4 segment. In contrast, decreases in galanin-IR were observed in the L1 segment. The number of galanin-IR cells increased (P < or = 0.001) in the L1 and S1 dorsal root ganglia (DRG) after SCI. In all DRG examined (L1, L2, L6, and S1), the percentage of bladder afferent cells expressing galanin-IR significantly increased (4-19-fold) after chronic SCI. In contrast, galanin expression in nerve fibers in the urinary bladder detrusor and urothelium was decreased or eliminated after SCI. Expression of the neurotrophic factors nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) was altered in the spinal cord after SCI. A significant increase in BDNF expression was present in spinal cord segments after SCI. In contrast, NGF expression was only increased in the spinal segments adjacent and rostral to the transection site (T7-T8), whereas spinal segments (T13-L1; L6-S1), distal to the transection site exhibited decreased NGF expression. Changes in galanin expression in micturition pathways after SCI may be mediated by changing neurotrophic factor expression, particularly BDNF. These changes may contribute to urinary bladder dysfunction after SCI.