Pathophysiology of idiopathic detrusor instability and detrusor hyper-reflexia. An in vitro study of human detrusor muscle.
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.
Kinder
R B
RB
Department of Urology, Leicester General Hospital.
Mundy
A R
AR
D000109:Acetylcholine / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D006801:Humans; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects* / Q000503:physiopathology; D012018:Reflex; D013779:Tetrodotoxin / Q000494:pharmacology; D001743:Urinary Bladder / Q000187:drug effects / Q000503:physiopathology*; D001745:Urinary Bladder Diseases / Q000503:physiopathology
D013779:Tetrodotoxin; D001285:Atropine; D000109:Acetylcholine