Introduction: Normal and abnormal bladder contractions are principally mediated by acetylcholine released from postganglionic parasympathetic nerves. Since amikacin was reported to affect neurotransmission by a prejunctional mechanism, we investigated the effect of amikacin on isolated detrusor smooth muscle contraction to further evaluate its potential relaxant properties. Materials and Methods: Detrusor smooth muscle obtained from 15 rats and 8 patients undergoing surgery were studied through measurement of isometric muscular contraction induced with electrical field stimulation (EFS) (10–60 Hz), carbachol (10–7 to 10–3M) and nicotine (10–7 to 10–3M) in the presence or absence of 1 mM amikacin in a low-Ca medium. Results: Amikacin (1 mM) significantly reduced EFS-induced contraction of isolated rat and human detrusor muscle by 33 ± 6.57% (p < 0.005) and 40 ± 1.14% (p < 0.001), respectively. Contraction was restored after addition of calcium chloride (1 mM). The effect of amikacin was comparable to that of magnesium ions. Rat and human detrusor contractile response to nicotine was inhibited by 70 ± 8.27% (p < 0.001) and 64 ± 14.09% (p < 0.01) after the addition of amikacin (1 mM), while no significant effect was observed on carbachol-induced stimulation. Conclusion: Amikacin significantly inhibited detrusor contraction evoked by prejunctional stimulation in vitro, suggesting a depressant effect on autonomic neurotransmission in urinary bladder.

Keywords:
Amikacin, Detrusor muscle, Contraction, Autonomic neurotransmission
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© 2008 S. Karger AG, Basel
2008
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