Objective To investigate the effect of partial bladder outlet obstruction on detrusor blood¯ow and oxygen tension (PdetO 2 ) in female pigs. Materials and methods Detrusor-layer oxygen tension and blood¯ow were measured using oxygen-sensitive electrode and radiolabelled microsphere techniques in ®ve female Large White pigs with a partial urethral obstruction and in ®ve sham-operated controls. The effects of chronic outlet obstruction on bladder weight, and cholinergic nerve density and distribution, are also described. Results In the obstructed bladders, blood¯ow and oxygen tension were, respectively, 54.9% and 74.3% of control values at low bladder volume, and 47.5% and 42.5% at cystometric capacity. Detrusor blood¯o w declined by 27.8% and 37.5% in the control and obstructed bladders, respectively, as a result of bladder ®lling, whilst PdetO 2 did not decrease in the controls, but fell by 42.7% in the obstructed bladders. Bladder weight increased whilst cholinergic nerve density decreased in the obstructed animals. Conclusion In pigs with chronic bladder outlet obstruction, blood¯ow and oxygen tension in the detrusor layer were lower than in control animals. In addition, increasing detrusor pressure during ®lling caused signi®cantly greater decreases in blood¯ow and oxygen tension in the obstructed than in the control bladders.
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.
This document should be used as a basis for appropriate evaluation and timely surveillance of the various neuro-urologic conditions that affect children.
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