Gastrointestinal motor and myoelectric correlates of motion sickness

The objectives of this study were to characterize the digestive tract motor and myoelectric responses associated with motion sickness. Twenty-two cats (1.5-3.0 kg) were chronically implanted with force transducers and electrodes on the stomach and small intestine. Motion sickness was activated by vertical oscillation (VO) at ±0.5 g and identified as salivation, licking, or vomiting. Vomiting was initiated chemically by UK-14304 (2.5-15 μg/kg iv) or CuSO₄ (10-50 mg ig). We found that VO caused vomiting (45% of trials), a decrease in gastrointestinal (GI) motility (69% of trials), salivation or licking (59% of trials), bradygastria (39% of trials), retrograde giant contraction (RGC, 43% of trials), giant migrating contraction (GMC, 5% of trials), and defecation (18% of trials). The decrease in GI motility occurred with (62% of trials) or without (69% of trials) vomiting. Motion sickness was accompanied by bradygastria (52% of trials) and decreased GI motility (70% of trials). Similar events occurred after CuSO₄ and UK-14304, but the incidences of responses after CuSO₄ were less frequent, except for vomiting, RGC, and GMC. UK-14304 never caused GMCs or defecation. The magnitude and velocity of the RGC were the same during all emetic stimuli, and RGCs never occurred without subsequent vomiting. Supradiaphragmatic vagotomy (n = 1) or atropine (n = 2,10 or 50 μg/kg iv) blocked the RGC, but not vomiting; due to VO. We concluded that 1) oculovestibular stimulation causes digestive tract responses similar to other types of emetic stimuli, 2) decreased GI motility and bradygastria may be physiological correlates of the motion sickness, and 3) motion sickness may not be dependent on any specific GI motor or myoelectric response.