Qualitative and quantitative ultrastructural studies on the rabbit detrusor following partial bladder outlet obstruction indicate the necessity of morphometry in evaluating structure of the dysfunctional detrusor. This report presents a review of the issues involved in such morphometry, as a prelude to presentation of a comprehensive protocol for this purpose in a subsequent report. In the present report, obstructive changes in the structurc of smooth muscle are reviewed, the parameters that should be evaluated are defined, the limitations of detrusor morphometry are presented, and the guidelines for a meaningful morphometric protocol for use in future studies on the dysfunctional detrusor are outlined.Keg words: urinary bladder, detrusor, obstruction, histology, electron microscopy
INTRODUCTIONIt is known that partial bladder outlet obstruction, whether acute and transient, episodic, of short duration or longstanding, results in alteration of detrusor voiding function. It is also known that relief of clinical obstruction is not necessarily followed by restoration of normal detrusor voiding function [Andersen, 1976; Apple, 1981; Styles et al., 19861. This has led to uncertainty about the validity of clinical criteria upon which such intervention has traditionally been based.Our recent qualitative ultrastructural study in a rabbit model revealed that partial bladder outlet obstruction leads to changes in the muscular, interstitial, and neural compartments of the detrusor [Elbadawi et al., 1989bl. These changes varied in nature (and apparently also degree) with the duration of obstruction, and were not completely reversed following its relief. It thus became obvious that the various changes observed need to be quantitated in order to define accurately their chronologic evolution and extent of reversibility . Our subsequent quantitative analysis of the same material [Meyer et al., 1989a,b] led to several important observations on the basis of which we proposed a working hypothesis on the structural basis of detrusor dysfunction in our rabbit model [Elbadawi et al., 1989al. More importantly, our quantitative analysis confirmed our suspicions (based on a