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Detrusor instability in prostatic obstruction in relation to urethral opening pressure
Author(s) -
Cucchi A.
Publication year - 1990
Publication title -
neurourology and urodynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 90
eISSN - 1520-6777
pISSN - 0733-2467
DOI - 10.1002/nau.1930090103
Subject(s) - medicine , urology , muscle hypertrophy , detrusor muscle , detrusor instability , urethra , pathological , denervation , bladder outlet obstruction , reflex , urinary bladder neck obstruction , urinary bladder , prostate , urinary incontinence , cancer
Forty males with bladder outflow obstruction from benign prostatic hypertrophy (BPH)—20 with unstable bladders and 20 with stable ones—were studied. All of these patients have been assessed both clinically and urodynamically. The presence of instability was found to be associated with a higher urethral opening pressure as well as to involve important changes in voiding dynamics, i.e., an increased velocity of shortening of the contracting detrusor and, most likely, an actively increased mechanical capability of the bladder smooth muscle to generate external voiding power. It seems that the link between an increased opening pressure and the presence of instability, with the consequent changes in voiding dynamics, can be well explained 1) by the theory that obstructive detrusor instability is a denervation supersensitivity phenomenon or even 2) by a pathological urethrovesical reflex, activated by abnormal afferent stimuli from an anatomically altered prostatic urethra. Both hypotheses are discussed herein. No correlation was found between the severity of detrusor trabeculation and the presence of instability. Such a feature is believed to depend on the aforementioned increase in the muscle mechanical capability of the detrusor. This might lessen the need for bladder smooth muscle hypertrophy (as a force generator) to develop in response to infravesical obstruction and thereby even the chance for collagen fibers to be produced by hypertrophic smooth muscle cells.

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