Ureteral ischemia model: an explanation of ureteral dysfunction after chronic obstruction.

Abstract

Many models of smooth muscle ischemia have been developed to explain organ insufficiency or failure. Ureteral decompensation may also be described in these terms. We anticipate that ureteral ischemia will result from overdistention brought about by obstruction. A preliminary model of an ischemic ureter is described herein. Six female New Zealand rabbits were used for this study. All had their left ureters surgically ligated at the level of the urinary bladder. The right ureters served as controls. In the acute-phase group, the ureters were reexplored 2 weeks after creation of obstruction. The other three rabbits were explored 3 weeks later. A laser Doppler needle was used to measure tissue perfusion with bilateral measurements of the renal artery and vein; renal parenchyma; renal pelvis; ureteropelvic junction; upper, mid, and lower ureter; and the lateral wall of the bladder. Baseline and postobstructive measurements of tissue perfusion were collected. In both the acute and chronic obstruction groups, there was a demonstrable drop-off in perfusion of the ureteral wall. The increased wall tension in the obstructed ureter results in a significant decrease in smooth muscle perfusion. This ischemia may result in the same functional and histologic changes that occur in other smooth muscle organs deprived of normal blood flow. Ultimately, poor outcomes of some restorative/reconstructive operations on the ureter may be explainable in terms of smooth muscle ischemia.