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Autonomic function and plasma catecholamines following stressful sensory stimuli
1Space Biomedical Research Institute, National Aeronautics and Space Administration, Johnson Space Center, Houston, TX.
Aviation, Space, and Environmental Medicine
|October 1, 1993
Summary
Epinephrine levels during motion sickness did not decrease with adaptation but higher epinephrine indicated greater resistance to motion. Drug interventions did not alter autonomic responses, suggesting non-catecholaminergic pathways are involved.
Area of Science:
- Neuroscience
- Autonomic Nervous System Research
- Human Physiology
Background:
- Motion sickness involves nausea and autonomic nervous system (ANS) responses.
- The role of epinephrine (a stress hormone) in motion sickness and adaptation is not fully understood.
Purpose of the Study:
- To investigate the role of epinephrine in autonomic nervous system function during motion sickness.
- To determine if repeated exposure alters epinephrine responses and if these responses correlate with motion sickness resistance.
Main Methods:
- Peripheral epinephrine levels were measured during motion sickness testing.
- Subjects underwent repeated exposure to assess adaptation.
- Pharmacological interventions (dexamethasone, scopolamine plus amphetamine) were used to modulate catecholaminergic function.
Main Results:
- Peripheral epinephrine levels did not significantly decrease with repeated exposure to the motion stressor.
- Higher epinephrine elevations in response to nausea correlated with increased resistance to stressful motion stimuli.
- Drug interventions did not alter autonomic nervous system function or nausea, suggesting peripheral catecholamine receptors are not the primary mediators.
Conclusions:
- Epinephrine response to motion sickness may predict an individual's resistance to stressful motion.
- These findings suggest a potential peripheral marker for an underlying central mechanism in motion sickness.