Abstract

AbstractPartial outlet obstruction of the rabbit urinary bladder was induced in New Zealand rabbits through surgical introduction of a silk ligature distal to the urethrovesicular junction. The consequence of this intervention is acute overdistension followed by severe bladder wall hypertrophy. In conjunction with physiological experiments, two additional animals were generated for histological evaluation at each of three time intervals after partial obstruction (1, 7, and 14 days), as well as six sham‐operated and two normal subjects. Bladders were fixed in Bouin's fluid and processed routinely for paraffin embedment. Sections were stained with hematoxylin and eosin (H&E), periodic acid Schiff (PAS), and elastin stains, and Mallory's triple stain for connective tissue (CT). The results of this present study confirm and significantly expand previous reports of CT hypertrophy after partial outlet obstruction. After 14 days of partial obstruction the elastin stains showed a peculiar welldefined lamina of elastin buried in the wall of the bladder. In 7‐day animals, the lamina is either buried as in 14‐day bladders, covered with bands of collagenous CT, or associated with the serosa. The lamina is confined to serosa in normal and sham operated animals and in partially obstructed animals, 24 hr after surgery. In normal and sham‐operated animals the elastic lamina is always found to be uninterrupted. In 1‐, 7‐, and 14‐day obstructed animals, the lamina is typically observed to be broken. The elastic lamina is part of the serosa rather than part of the bladder, and it accompanies the mesothelium wherever it is found. Nonetheless, it is clear from these experiments that the serosa becomes involved in the response of the bladder to the obstructive insult, and a fibrotic reaction of the serosa contributes to the thickening of the wall of the hypertrophic bladder. By using this elastic lamina as a marker, CT hypertrophy can be classified as either intrinsic (that within the original bladder wall) or extrinsic (that within the serosal comartment). Although the precise sources of these additional materials are not known at present, hypotheses are suggested. These distinctions may be important in determining the specific cellular and tissue causes of decreased bladder function that are characteristic of certain bladder pathologies.

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