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 to create an ischemic ureter is described herein. Six white New Zealand female 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 all reexplored 2 weeks postobstruction. Exploration of the other rabbits was delayed for 3 more weeks. A laser Doppler needle (Transonics Inc.) was used to measure tissue perfusion in the rental artery, renal vein, renal parenchyma, renal pelvis, ureteropelvic junction, upper ureter, mid ureter, lower ureter, and lateral wall of the bladder. Baseline and postobstructive measurements of tissue perfusion were collected and compared. In both the acute and the chronic obstruction groups, there was a demonstrable drop-off in perfusion of the ureteral sidewall. A more notable loss of perfusion was seen in the distal ureter. 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. Ultimately, the poor outcomes of some restorative/reconstructive procedures on the ureter may be explained in terms of smooth muscle ischemia.