The Functional Effect of Mild Outlet Obstruction on the Rabbit Urinary Bladder

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Abstract
Bladder outlet obstruction has been the subject of numerous studies. In previous studies on severe obstruction, the initial response of the bladder has been to produce an acute overdistension of the bladder resulting in severe tissue damage and functional disorders. This is quite different from the slow onset of outlet obstruction seen in association with benign prostatic hypertrophy (BPH). The present study describes the functional effect of mild outlet obstruction created in a rabbit model, and compares it to a previously described model of severe obstruction. Mild bladder outlet obstruction was created by placing a silicon sleeve (inner circumference 30 mm.) around the bladder neck of mature male NZW rabbits. Individual groups of rabbits were studied at one, seven, and 14 days following the creation of the outlet obstruction. The following studies were performed on each group of rabbits: in vivo and in vitro cystometry, field stimulation and cholinergic stimulation using the in vitro whole bladder model. In addition, the tissue concentration of ATP (adenosine triphosphate) and CP (creatine phosphate) and the muscarinic receptor density were determined. The obstructed bladders showed no significant cystometric difference at one day, but revealed a marked decrease of compliance and capacity at one and two weeks. Unlike the response to severe outlet obstruction, there was no initial acute overdistension of the bladder wall. Although the ability of the obstructed bladders to generate intravesical pressure in response to both field stimulation and bethanechol did not decrease, the ability of both forms of stimulation to empty the obstructed bladders was markedly impaired. The response to field stimulation was reduced to a significantly greater extent than the response to bethanechol, indicating neuronal damage. The muscarinic receptor number per bladder was increased above control at all time periods. The intracellular concentration of ATP and CP in the obstructed bladders was similar to that of control. Our present model of mild obstruction was not accompanied by a massive increase in tissue mass nor was there an overdistension of the detrusor; thus, this model would be a more suitable model for the study of clinical outlet obstruction.