Influence of mosapride citrate on gastric motility and autonomic nervous function: evaluation by spectral analyses of heart rate and blood pressure variabilities, and by electrogastrography
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Mosapride citrate selectively acts on serotonin (5-HT4) receptors, thus accelerating gastrointestinal motility via acetylcholine. However, few studies have evaluated the influence of mosapride citrate on autonomic nervous activity and hemodynamics. Methods: The changes in autonomic nervous activity, QT interval, and QT dispersion resulting from the administration of mosapride citrate were studied. Blood pressure, electrocardiograms (ECGs), percutaneous electrogastrograms (EGGs), and ultrasonography were recorded in 20 healthy adult volunteers before and after mosapride citrate (10 mg) was administered. Autonomic nervous activity was evaluated by spectral analyses of heart rate and blood pressure variabilities. Serial changes in low-frequency components (LF, 0.04–0.15 Hz), high-frequency components (HF, 0.15–0.40 Hz), and the LF/HF ratio were investigated. Results: The mean peak power of EGG increased significantly, from 86 ± 34 μV to 131 ± 49 μV, after the administration of mosapride citrate (P < 0.05). Gastric emptying significantly increased after the administration of mosapride citrate (P < 0.05). However, neither blood pressure nor heart rate changed significantly after the drug was administrated. In addition, spectral analyses of heart rate and blood pressure variabilities showed no significant changes in autonomic nervous activity parameters, QT intervals, or QT dispersions. Conclusions: Mosapride citrate increased gastric motility and emptying without influencing autonomic nervous activity, suggesting that it may be very useful for elderly patients or patients with autonomic imbalance.
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