Aviation, space, and environmental medicine · 1995
Effects of dimenhydrinate on gastric tachyarrhythmia and symptoms of vection-induced motion sickness.
Клиническое исследованиеКонтролируемое клиническое исследованиеСтатьяПоддержка правительства СШАНазвание и аннотация: Перевод в очереди
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Muth E R, Jokerst M, Stern R M, Koch K L
Аннотация
BACKGROUND: Previous research in our laboratory has shown that symptoms of motion sickness are accompanied by the loss of normal 3 cpm activity and the development of tachyarrhythmia in the electrogastrogram (EGG).
HYPOTHESIS: We hypothesized that dimenhydrinate would prevent the development of gastric tachyarrhythmia and reduce symptoms of motion sickness.
METHODS: Twenty health volunteers were tested in a counter-balanced, within-subject, double-blind design. Subjects were exposed to a rotating optokinetic drum to induce vection after receiving either dimenhydrinate (100 mg) or a placebo on two separate occasions. EGG's were recorded immediately before ingestion of capsules, 1 h after ingestion, and during rotation. Motion sickness symptom reports (SSMS) were obtained prior to and during rotation.
RESULTS: The average SSMS score was 5.9 points higher after placebo administration than after dimenhydrinate administration (t[19] = 4.87, P < 0.001). Significantly more subjects requested early termination of the rotating drum due to severe symptoms after placebo administration than after dimenhydrinate administration (McNemar's chi 2[1] = 6.00, p < 0.05). Drowsiness reports were significantly higher after dimenhydrinate administration than after placebo administration (t[19] = 2.65, p < 0.05). Analysis of EGG's showed a significant decrease in normal 3 cpm and tachyarrhythmic activity after dimenhydrinate, but no change after placebo (SR[19] = 53, p < 0.02 and SR[19] = 68, p < 0.01 respectively). During drum rotation gastric tachyarrhythmias increased significantly in the placebo condition (SR[18] = -0.61.5, p < 0.01), but not in the dimenhydrinate condition. EGG's were not significantly different between conditions.
CONCLUSIONS: We conclude that dimenhydrinate reduced motion sickness symptoms at least in part by depressing central nervous system activity and possibly by suppressing abnormal gastric myoelectric activity.
HYPOTHESIS: We hypothesized that dimenhydrinate would prevent the development of gastric tachyarrhythmia and reduce symptoms of motion sickness.
METHODS: Twenty health volunteers were tested in a counter-balanced, within-subject, double-blind design. Subjects were exposed to a rotating optokinetic drum to induce vection after receiving either dimenhydrinate (100 mg) or a placebo on two separate occasions. EGG's were recorded immediately before ingestion of capsules, 1 h after ingestion, and during rotation. Motion sickness symptom reports (SSMS) were obtained prior to and during rotation.
RESULTS: The average SSMS score was 5.9 points higher after placebo administration than after dimenhydrinate administration (t[19] = 4.87, P < 0.001). Significantly more subjects requested early termination of the rotating drum due to severe symptoms after placebo administration than after dimenhydrinate administration (McNemar's chi 2[1] = 6.00, p < 0.05). Drowsiness reports were significantly higher after dimenhydrinate administration than after placebo administration (t[19] = 2.65, p < 0.05). Analysis of EGG's showed a significant decrease in normal 3 cpm and tachyarrhythmic activity after dimenhydrinate, but no change after placebo (SR[19] = 53, p < 0.02 and SR[19] = 68, p < 0.01 respectively). During drum rotation gastric tachyarrhythmias increased significantly in the placebo condition (SR[18] = -0.61.5, p < 0.01), but not in the dimenhydrinate condition. EGG's were not significantly different between conditions.
CONCLUSIONS: We conclude that dimenhydrinate reduced motion sickness symptoms at least in part by depressing central nervous system activity and possibly by suppressing abnormal gastric myoelectric activity.