EFFECTS OF MOTION SICKNESS AND ANTIMOTION SICKNESS DRUGS ON GASTRIC FUNCTION

Citation
Jj. Stewart et al., EFFECTS OF MOTION SICKNESS AND ANTIMOTION SICKNESS DRUGS ON GASTRIC FUNCTION, Journal of clinical pharmacology, 34(6), 1994, pp. 635-643
Citations number
36
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00912700
Volume
34
Issue
6
Year of publication
1994
Pages
635 - 643
Database
ISI
SICI code
0091-2700(1994)34:6<635:EOMSAA>2.0.ZU;2-G
Abstract
This study examined the effects of motion sickness and antimotion sick ness drugs on gastric emptying (GE). Drugs were tested in normal and m otion sick subjects. To induce motion sickness, subjects performed hea d movements while seated in a rotating chair. Gastric emptying of liqu id (300 mt) was determined by nuclear medicine techniques, whereas gas tric electrical activity, the electrogastrogram (EGG), was monitored f rom surface (cutaneous) electrodes positioned over the abdominal area. Gastric emptying was severely inhibited at the peak of motion sicknes s symptoms, but returned to normal 15 minutes later when symptoms abat ed. In normal (non-motion sick) subjects intramuscular (IM) scopolamin e (0.1 mg) and IM promethazine (25 mg) inhibited GE, whereas erythromy cin ethylsuccinate (EES) suspension (200 mg) given orally increased GE . When administered to motion sick subjects, IM scopolamine and IM pro methazine added slightly, but not significantly, to the inhibition of GE already present. Oral EES did not significantly alter GE in motion sick subjects. Although EGG frequency remained within normal limits(si milar to 2.5-3.5 cpm) after liquid ingestion in both normal and motion sick subjects, EGG amplitude was differentially affected in the two g roups. Electrogastrogram amplitude increased twofold to fourfold after liquid ingestion in normal, but not in motion sick subjects. The resu lts suggest that (1) maximal inhibition of GE is coincident with peak motion sickness symptoms, (2) both IM scopolamine and IM promethazine inhibit GE in normal subjects, but do not add significantly to the inh ibition of GE already established during motion sickness, (3) orally a dministered erythromycin enhances GE in normal, but not in motion sick subjects, and (4) the normal stimulatory effect of liquid ingestion o n gastric motility does not occur in motion sick subjects. Both motion sickness and parenterally administered antimotion sickness drugs are potential sources of inhibited GE in space.