Vascular response of the rabbit bladder to short term partial outlet obstruction.
Partial bladder outlet obstruction of the rabbit bladder results in a rapid increase in mass characterized by remodeling of the bladder wall. In this study we investigated the effect of partial outlet obstruction on microvessel density and distribution in the bladder wall immunohistochemically using CD31 as a marker for vascular endothelium, and on blood flow using a fluorescent microsphere technique. Transverse sections of bladder wall were examined after 0 (unobstructed), 1, 3, 5, 7, and 14 days of obstruction. The microvasculature of obstructed rabbit bladder mucosa and detrusor smooth muscle apparently increased relative to augmentation of these compartments, while new vessels appeared in the thickening serosa. These vascular changes correlated with results showing that, at 1 week after obstruction, blood flow (ml/min/g tissue) to the mucosa and detrusor was unchanged. Thickening of the serosa, apparent after 1 day of obstruction, began before its vascularization. Then, 1 week post-obstruction, there was significant microvessel formation in the transition region between the detrusor smooth muscle and the increasing serosa; after 2 weeks, the entire serosa was vascularized. The vascularization of the muscle-serosal transition region and then the remaining serosa apparently precedes fibroblast differentiation, providing blood supply and thus metabolic support for this process. All obstructed rabbit bladders in this study were in a state of compensated function based on their weights. Our working hypothesis is that blood flow per unit tissue mass is normal in compensated obstructed bladders, thus allowing for normal contractile function and cellular metabolism. The results of this study indicate the presence of an augmented microvasculature in compensated obstructed rabbit bladders that provides adequate blood perfusion for normal function.
Chichester
P
P
Division of Basic and Pharmaceutical Science, Albany College of Pharmacy, NY 12208, USA.
Lieb
J
J
Levin
S S
SS
Buttyan
R
R
Horan
P
P
Levin
R M
RM
D000818:Animals; D004730:Endothelium, Vascular / Q000737:chemistry / Q000473:pathology; D006965:Hyperplasia; D006984:Hypertrophy; D008297:Male; D008863:Microspheres; D009130:Muscle, Smooth; D009929:Organ Size; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis / Q000276:immunology; D011817:Rabbits; D012039:Regional Blood Flow; D001743:Urinary Bladder / Q000098:blood supply* / Q000473:pathology; D001748:Urinary Bladder Neck Obstruction / Q000473:pathology* / Q000503:physiopathology; D019459:Urothelium / Q000098:blood supply / Q000473:pathology / Q000502:physiology
D019408:Platelet Endothelial Cell Adhesion Molecule-1