Role of plasma vasopressin as a mediator of nausea and gastric slow
wave dysrhythmias in motion sickness.
Kim, Michael S., William D. Chey, Chung Owyang, William L. Hasler.
Division of Gastroenterology, Department of Internal Medicine,
University of Michigan Medical Center, Ann Arbor, MI, 48109
APStracts 3:0234G, 1996.
The possible role of vasopressin in nausea and gastric dysrhythmias in
motion sickness was tested by electrogastrography in 14 subjects
during circular vection (60o/sec) and vasopressin infusion.
Tachygastria was expressed as the signal percent >4.5
cycles/min. Vection evoked nausea scores of 2.6 0.2 (0=none to
3=severe) in 10 subjects with increases in tachygastric activity (15
2 to 45 3%) and plasma vasopressin (4.5 1.5 to 8.4 2.5 pg/ml), that
were blocked by atropine but not indomethacin. 4 asymptomatic
subjects had no tachygastria or vasopressin release. Vasopressin at
0.2 U/min (plasma level=322.1 10.3 pg/ml) evoked nausea (2.6 0.4) and
increases in tachyarrhythmic activity (41 5%) that were blunted by
atropine but not indomethacin. There were no differences in nausea or
dysrhythmias with vasopressin infusion in subjects who noted nausea
during vection versus those who did not. To conclude, vection evokes
nausea, dysrhythmias, and vasopressin release in motion sickness
-susceptible humans via cholinergic, prostaglandin-independent
pathways. Supraphysiologic vasopressin infusions evoke nausea and
dysrhythmias by similar pathways to equal degrees in motion sickness
-susceptible and resistant subjects. Thus central but not peripheral
actions of vasopressin may contribute to nausea and slow wave
disruption with vection. Blunting of both the release and action of
vasopressin by atropine may explain its beneficial action in motion
sickness.
Received 2 October 1995; accepted in final form 2 October 1995.
APS Manuscript Number G424-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996