1997
DOI: 10.1152/ajpgi.1997.272.4.g853
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Role of plasma vasopressin as a mediator of nausea and gastric slow wave dysrhythmias in motion sickness

Abstract: The possible role of vasopressin in nausea and gastric dysrhythmias in motion sickness was tested by electrogastrography in 14 subjects during circular vection (60 degrees/s) 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 indo… Show more

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Cited by 75 publications
(98 citation statements)
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“…Specifically, indomethacin does not prevent induction of tachygastria by circular vection indicating the lack of participation by endogenous prostaglandins (Hasler et al, 1995a). Rather, gastric myoelectric rhythm disturbances in motion sickness may be mediated in part by cholinergic pathways and vasopressin release (Kim et al, 1997). In the present investigation, nitroglycerin and sildenafil had no prophylactic effect on circular vection-induced dysrhythmias.…”
Section: Discussioncontrasting
confidence: 69%
“…Specifically, indomethacin does not prevent induction of tachygastria by circular vection indicating the lack of participation by endogenous prostaglandins (Hasler et al, 1995a). Rather, gastric myoelectric rhythm disturbances in motion sickness may be mediated in part by cholinergic pathways and vasopressin release (Kim et al, 1997). In the present investigation, nitroglycerin and sildenafil had no prophylactic effect on circular vection-induced dysrhythmias.…”
Section: Discussioncontrasting
confidence: 69%
“…Although this does not exclude a role for vasopressin in the genesis of nausea in intact individuals, it is a clear that a rise in plasma vasopressin is not essential for the production of nausea under all circumstances and taken together with the studies of vasopressin infusion and plasma levels could indicate that vasopressin requires an additional factor(s) to be present for the induction of nausea when it is released at a lower concentration. This appears to be particularly likely in the case of the circular vection model of motion sickness (Kim et al, 1997). …”
Section: Neurohypophyseal Hormonal Secretions and Gastric Dysrhythmiamentioning
confidence: 96%
“…Plasma vasopressin levels appear to increase slightly before or at the onset of nausea (Miaskiewicz et al, 1989;Koch et al, 1990b). Administration of vasopressin at supraphysiological doses produced nausea in humans, but when vasopressin was infused to match the plasma level during nausea induced by motion nausea was not reported (Kim et al, 1997). Additionally, apomorphine induces nausea in patients with idiopathic diabetes insipidus despite the absence of an increase in plasma vasopressin (Nussey et al, 1988).…”
Section: Neurohypophyseal Hormonal Secretions and Gastric Dysrhythmiamentioning
confidence: 99%
“…Myoelectrical abnormalities of the stomach have been recorded in patients with unexplained nausea and vomiting, during pregnancy, in motion sickness, and in patients with anorexia nervosa; this dysrhythmia seems to correlate with antral hypomotility and delayed gastric emptying [11]. Several peptide hormones induce gastric dysrhythmia, including glucagon [12], gastrin, secretin, somatostatin [13], CCK [14], vasopressin [15], and epinephrine [16]. Finally, gastric emptying is usually studied by means of scintigraphy, although ultrasound has been demonstrated to be a reliable, noninvasive method [17].…”
Section: Introductionmentioning
confidence: 99%