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Ultrasound examination of the abdominal cavity is part of the baseline diagnostics of urinary tract diseases. Dilatation of the pelvicalyceal system is one of the most frequent findings. In ultrasonography of the urinary tract there are, however, some images of anatomical anomalies of the pelvicalyceal system which should not be consider as abnormal. In the study we analysed 920 ultrasound examinations of the urinary tract. Of all the ultrasound images only those with isolated dilatation of the renal pelvises and calices were selected (130 cases). Ampulla-shaped and/or external pelvises, isolated calices or both abnormalities were disclosed in 104, 46 and 20 cases, respectively. In about one-third of patients additional examinations (voiding cystography, intravenous urography, renal scyntygraphy) were performed which revealed normal anatomy of the urinary tract and disorders of urine flow in 80% and 20% of patients, respectively. In conclusion, the study implies that not all dilatation of the pelvicalyceal system structures signifies urine retention, although in the event of further doubt, there is a need for additional diagnostics.
The study investigated the mechanisms through which the hyperosmolarity might induce detrusor overactivity (DO). We compared the bladder activity in response to partial and complete blockade of TRPV1-6 and TRPA1 receptors. Experiments were performed on 42 rats. DO was induced by using hyperosmolar saline. All animals were randomly divided into six groups. The measurements represent the average of five bladder micturition cycles. Hyperosmolar saline induced DO. The complete blockade of TRPV1-6 and TRPA1 prevented DO. The partial blockade of TRPV1 didn't prevented DO. In the voiding phase periodical bladder contractions complexes occurred leading to slow urine flow due to bladder distension. Ruthenium red and capsaicin resulted in complete disorganisation of detrusor muscle contractility impairing urine voiding and leading to constantly lasting urine retention in healthy rats. Conclusions: hyperosmolar-induced DO is mediated by TRPV and TRPA1 channels; the hyperosmolar stimuli of urinary bladder might be transmitted mostly via ruthenium red sensitivity pathway.
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