Ureteral obstruction (UO) is one of the most common problems confronting the urologist. Although large amounts of animal and clinical research have been done, the pathophysiologic mechanisms accompanying UO are not fully elucidated. Most of our knowledge on UO has been derived from experimental studies in a variety of animal models. Both antenatal and postnatal UO models have been developed mainly by ligation of the ureter or by burying the ureter into the psoas muscle. Most experimental studies have focused on short-term complete ureteral obstruction. The long-term effects of partial ureteral obstruction have been less intensively studied. It is now clear that obstructive nephropathy is not a simple result of mechanical impairment to urine flow but a complex syndrome resulting in alterations of both glomerular hemodynamics and tubular function caused by the interaction of a variety of vasoactive factors and cytokines that are activated in response to UO. Leukocyte infiltration appears to play an important role in obstructive nephropathy suggesting that UO also has an immunological component. Growth factors such as platelet-derived growth factor, transforming growth factor-beta, epidermal growth factor and insulin-like growth factor I may all play a role in the development and progression of fibrotic and sclerotic changes in the obstructed kidney. At present, the selection of patients with congenital hydronephrosis for operative treatment is controversial. Studies in animals and patients have shown that partial unilateral UO does not always cause a loss of renal function or progression in urinary tract dilation during long-term follow-up. The implications of UO continue to raise many questions and further work is necessary to achieve a better understanding of the pathogenesis in obstructive nephropathy.

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Prostanoids exert physiological effects on ureteral contractility that may lead to pressure changes and pain during obstruction. In the present study, we examined whether (1) obstruction changes the expression of the two cyclooxygenase (COX) isoforms, COX-1 and COX-2 in human and rat ureters and (2) administration of a selective COX-2 inhibitor influences the pelvic pressure change after experimental ureteral obstruction. Rats were subjected to bilateral ureter obstruction. Ureters were removed and dissected into a proximal dilated and distal non-dilated segment. RNA and protein were extracted and analyzed for cyclooxygenase expression by quantitative polymerase chain reaction and Western blotting. Human ureter samples were obtained from patients undergoing radical nephrectomy. Rat and human ureteral samples were processed for immunohistochemistry. COX-1, but not COX-2 mRNA, was readily detected in the normal rat ureter. COX-2 mRNA and protein expression was increased in the proximal dilated ureter compared to distal non-dilated ureter. This increased COX-2 expression was associated with increased urinary prostaglandin E2 (PGE2) excretion after release of obstruction. Immunohistochemistry showed increased COX-2 labeling in surface epithelium and smooth muscle layers in both rat and human obstructed ureters compared to control ureters. Furthermore, contractile PGE2-EP1 and thromboxane TP receptors were expressed in ureteral smooth muscle. Systemic treatment with the COX-2 selective inhibitor parecoxib (5 mg/kg/day) attenuated the pelvic pressure increase during obstruction. In summary, COX-2 expression is significantly increased in the ureteral wall in response to obstruction in the rat and human ureter and COX-2 activity contributes to increased pelvic pressure after obstruction.

Fifty-six patients were investigated by repetitive cystometry in the supine or sitting position. The incidence of detrusor hyperreflexia and the circumstances under which it was found did not differ from previous studies. The cystometry data concerning volumes showed a remarkable degree of variability. Values for first sensation and maximal capacity could vary more than 500%. An increment from the first cystometry to the fourth was consistently found. The increments were most pronounced when cystometry with fast filling followed cystometry with medium filling regardless of the patient's position. The major factor in the changes is considered to be the patient's adaptation to the investigational situation. This finding might have major significance in the evaluation of drug studies where repeated cystometries with different time intervals are used.

Objectives To: (i) visualize the effect of sustained voluntary contractions on the anatomical configuration of the pelvic floor (PF) muscles using magnetic resonance imaging (MRI); (ii) examine the effect of ageing on the range of displacement of the PF contents secondary to contraction and simulating incontinence exercises; and (iii) introduce the concept of contractile change in volume ( ∆ PF-V) using three-dimensional (3D) reconstruction from axial, sagittal and coronal MRI. Subjects and methods Two groups of continent women volunteers, familiar with correct PF contraction, were evaluated. The mean ( SD ) age in group I was 34 (6) years and that of group II 55 (9) years; the mean parities were 0.7 and 2.2, respectively. MRI was conducted with the women supine and data were obtained in the axial, sagittal and coronal planes. In each plane, images were obtained with the PF relaxed and subsequently with the PF contracted over 10-20 s. Image processing was used to enhance the anatomical boundaries of the pelvic organs and to measure the displacement produced by the contraction. Displacements, observed between each image pair, were colourcoded to highlight the geometric differences between a relaxed and contracted PF and to facilitate measuring displacement. Data measured from each group were pooled and the range of motion expressed as the mean ( SD ), compared using Student's t -test. Results Digitally processed imaging allowed an accurate comparison between the relaxed and contracted PF, and highlighted the differences between them. From these views, the levator ani displaced the vagina asymmetrically in nine of the 11 older subjects, and in six of the 17 younger subjects. The values from the imaging in the sagittal and coronal plane for the two groups were: levator ani displacement, 7.4 (1.1) and 1.4 (0.2) cm ( P < 0.002), superior bladder wall, 4.2 (0.5) and 1.0 (0.1) cm ( P < 0.002). There were also significant differences in the range of displacement produced by voluntary PF contraction in the internal structures; external outlines did not reflect these changes. The maximum displacement of the gluteal surface in the coronal plane did not change significantly; in group I it was 3.9 (1.8) to 2.9 (0.7) cm. From the 3D re-construction, ∆ PF-V for the younger women was significantly larger, at 23.3 (3.9) mL ( P < 0.01) than in the older women, at 9.1 (4.4) mL. Conclusion The range of motion over which voluntary PF contractions displace the bladder and vagina is agedependent, being higher in younger than in older subjects. It remains to be established whether range of movement is a limitation caused by neuronal factors, decrease in muscle strength/mass, or the substitution of spaces with fat (restricting free movement), or other factors.