Background and Purpose: Many models of smooth muscle ischemia have been dev
eloped to explain organ insufficiency or failure. Ureteral decompensation m
ay also be described in these terms. We anticipate that ureteral ischemia w
ill result from overdistention brought about by obstruction. A preliminary
model of an ischemic ureter is described herein.
Materials and Methods: Six female New Zealand rabbits were used for this st
udy. All had their left ureters surgically ligated at the level of the urin
ary bladder. The right ureters served as controls. In the acute-phase group
, the ureters were reexplored 2 weeks after creation of obstruction, The ot
her three rabbits were explored 3 weeks later. A laser Doppler needle was u
sed to measure tissue perfusion with bilateral measurements of the renal ar
tery and vein; renal parenchyma; renal pelvis; ureteropelvic junction; uppe
r, mid, and lower ureter; and the lateral wall of the bladder. Baseline and
postobstructive measurements of tissue perfusion were collected.
Results: In both the acute and chronic obstruction groups, there was a demo
nstrable drop-off in perfusion of the ureteral wall.
Conclusion: The increased wail 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 m
uscle organs deprived of normal blood flow. Ultimately, poor outcomes of so
me restorative/reconstructive operations on the ureter may be explainable i
n terms of smooth muscle ischemia.