Drug therapy for detrusor hyperactivity: Where are we?

Wein, Alan J.

doi:10.1002/nau.1930040411

Cited by 17 publications

(1 citation statement)

References 73 publications

(17 reference statements)

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“…In addition, it occurs in the absence of any known dysfunction [3][4][5], Therapies for uninhibited contractions include oral drug therapy [6][7][8], instillation drug therapy [9,10] and chemical or surgical parasympa thetic nerve ablation [11,12], All therapies are directed at decreasing bladder contractile activity. In order to develop more effective therapies for uninhibited bladder contrac tions, we have developed an experimental model of reflex contractile activity (hyperre flexia) [13,14], Utilizing this model, we have compared the effectiveness of a variety of intravesically administered agents on hyper reflexia.…”

Section: Introductionmentioning

confidence: 99%

Experimental Hyperreflexia: Effect of Intravesical Administration of Various Agents

et al. 1991

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In anesthetized rabbits, we can induce a significant degree of spontaneous activity in the urinary bladder by placing a ligature around the proximal portion of the external urethra. Previous studies characterized the activity as primarily reflex in nature, since intravesical hexamethonium selectively inhibited the hyperreflexia. In this current study we determined the effect of intravesical administration of a variety of compounds to inhibit the induced hyperreflexia. The following agents were tested at concentrations of 1, 10, 100 and 500 μmol/l (intravesically): verapamil, cromakalim, nifedipine, diltiazem, and atropine; lidocaine was tested in 0.05, 0.5 and 5% solutions. The results are summarized as follows: (1) Lidocaine was the most effective agent tested, virtually eliminating both the amplitude and frequency of the spontaneous activity at the lowest concentration (0.5%). (2) Verapamil and nifedipine were somewhat more potent than cromakalim and diltiazem. Atropine sulfate was the least potent, inhibiting both the amplitude and frequency of the hyperreflexia by less than 50% at 500 μmol/l. (3) In all cases, the amplitude of the spontaneous activity was inhibited to a significantly greater degree than the frequency of the spontaneous activity. (4) In general, there was no effect of any of the agents on mean arterial pressure at 1 or 10 μmol/l. At 100 and 500 μmol/l, all agents except for lidocaine and cromakalim decreased arterial pressure. These two agents produced no consistent fall in blood pressure at any concentration. In conclusion, the acute hyperreflexic (rabbit) preparation provides a highly reproducible and consistent model for the study of the effect of drugs on hyperreflexia. The data presented in this report would indicate that the intravesical administration of antispasmodic (and other) agents might provide a useful method of treatment for this condition.

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Section: Introductionmentioning

confidence: 99%

Experimental Hyperreflexia: Effect of Intravesical Administration of Various Agents

et al. 1991

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Continuous urethral pressure measurement in women with unstable detrusor

Sørensen

Nørgaard

Djurhuus³

1986

Neurourology and Urodynamics

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To study the role of the urethra in bladder instability, we performed continuous urethrocystometry in 16 patients with verified unstable detrusor and found two qualitatively different pressure oscillations in the urethra: 1) continuous rhythmic pressure waves, characterized by frequency and pressure amplitude and 2) sudden and consistent urethral pressure drops of 35 cm H 2 0 occurring on average at mean time intervals of 3.5 seconds prior to the onset of the detrusor contraction. Simultaneous pelvic floor electromyographic (EMG) registration showed that the urethral pressure drop occurred either during decreased, unchanged, or increased pelvic floor activity. Restoration of the urethral pressure to its previous level was also unrelated to the pelvic floor EMG activity. Increased EMG activity at the onset of urethral pressure drops was not sufficient to suppress the urethral pressure drop, but could abolish the detrusor contraction.These findings suggest that the unstable detrusor is of a complex pathophysiological origin and involves both storage and micturition as well as detrusor and urethral function.

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Comparative effects of five different calcium channel blockers on the atropine‐resistant contraction in electrically stimulated rabbit urinary bladder

Andersson

Fovaeus

Morgan

et al. 1986

Neurourology and Urodynamics

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The effects of the calcium channel blockers nifedipine, verapamil, diltiazem, flunarizine, and lidoflazin on electrically induced contractions of isolated rabbit detrusor were compared in the absence and presence of muscarinic receptor blockade with scopolamine. All drugs had a depressant effect on the contractions both before and after scopolamine addition, nifedipine being the most potent of the calcium channel blockers. However, only nifedipine showed a significant preference for the nonmuscarinic part of the contraction, which was almost abolished at a concentration of M. It is concluded that combined muscarinic receptor and calcium channel blockade is an effective means of inhibiting bladder contraction. Differences between calcium channel blockers may be of importance in this respect.

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Drug therapy for detrusor hyperactivity: Where are we?

Cited by 17 publications

References 73 publications

Experimental Hyperreflexia: Effect of Intravesical Administration of Various Agents

Experimental Hyperreflexia: Effect of Intravesical Administration of Various Agents

Continuous urethral pressure measurement in women with unstable detrusor

Comparative effects of five different calcium channel blockers on the atropine‐resistant contraction in electrically stimulated rabbit urinary bladder

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