Pathophysiology of Idiopathic Detrusor Instability and Detrusor Hyper-reflexia
An in vitro Study of Human Detrusor Muscle
Article first published online: 21 NOV 2008
British Journal of Urology
Volume 60, Issue 6, pages 509–515, December 1987
How to Cite
KINDER, R. B. and MUNDY, A. R. (1987), Pathophysiology of Idiopathic Detrusor Instability and Detrusor Hyper-reflexia. British Journal of Urology, 60: 509–515. doi: 10.1111/j.1464-410X.1987.tb05031.x
- Issue published online: 21 NOV 2008
- Article first published online: 21 NOV 2008
Summary— Muscle strips from urodynamically normal bladders and from bladders exhibiting idiopathic detrusor instability or detrusor hyper-reflexia were compared under isometric conditions in an organ bath. Spontaneous contractions developed more often in unstable and hyper-reflexic muscle and were of greater amplitude, frequency and basal tension.
Electrical field stimulation caused a frequency-dependent contraction which was largely abolished by both tetrodotoxin (TTX) and atropine in all three muscle types. Comparison of their frequency response curves demonstrated a significantly greater sensitivity than that of unstable and hyper-reflexic muscle to low stimulation frequencies.
Acetylcholine caused a dose-related contractile response in all muscle types. There were no significant differences between the dose response curves of unstable and hyper-reflexic muscle, and those of normal muscle.
The results suggest that the pathophysiology of the involuntary detrusor contraction is common to both idiopathic detrusor instability and detrusor hyper-reflexia and that this is related to a disorder of an intrinsic neuromodulatory mechanism within the detrusor muscle.