pituitrin and Motion-Sickness

Stress hormones might be involved in motion sickness. The influence of loperamide on kinetosis-induced nausea and stress hormone release was investigated in a placebo-controlled, cross-over study.. Standardized rotation around the vertical axis combined with head movements was used to induce nausea 3 h after 16 mg loperamide or placebo (n = 8). Plasma antidiuretic hormone (ADH), adrenocorticotropic hormone (ACTH) and nausea ratings were investigated.. After loperamide nausea was significantly lower (P < 0.02). ACTH (P < 0.05) and ADH levels (P < 0.02) increased significantly in both settings, but were lower after loperamide.. The susceptibility to develop kinetosis-induced nausea and stress hormone release is decreased by loperamide, although the site of action remains speculative.

Topics: Adrenocorticotropic Hormone; Adult; Cross-Over Studies; Female; Humans; Loperamide; Male; Motion Sickness; Nausea; Receptors, Opioid, mu; Rotation; Single-Blind Method; Vasopressins

Arginine vasopressin (AVP) is considered as an etiologic hormone in motion sickness. However, the possible role of plasma AVP in motion sickness is still controversial. A number of studies have found a gender difference in susceptibility to motion sickness in humans and experimental animals, with female subjects being more susceptible. However, the existence of a gender difference in the AVP response to motion sickness is not known. This study was designed to verify the assumption that plasma vasopressin plays a role in motion sickness. Changes in plasma vasopressin were observed after motion sickness-inducing rotatory stimuli in both sexes in human subjects and rats receiving or not anti-motion-sickness treatments. Plasma vasopressin levels in motion sickness rats exhibited a decrease after rotation in female, but not in male rats. The vasopressin content of the pituitary increased in both sexes. Plasma vasopressin in rats of both sexes tended to increase after a 15-day adaptive training of rotation, but pituitary vasopressin content was not affected under this condition. In contrast, in human subjects, plasma vasopressin levels increased after rotation in all males, but not in females. When anti-motion-sickness drugs (domperidone 10 mg + flunarizine 5 mg) were administered, plasma vasopressin levels were elevated in both females and males. It is concluded that plasma vasopressin increases after motion sickness-induced stimulation provided subjects have become trained to motion sickness. These results do not support an etiologic role of plasma vasopressin in the genesis of motion sickness.

Topics: Adult; Animals; Domperidone; Dopamine Antagonists; Female; Flunarizine; Humans; Male; Motion Sickness; Physical Stimulation; Pituitary Gland; Rats; Rats, Sprague-Dawley; Rotation; Sex Characteristics; Species Specificity; Vasodilator Agents; Vasopressins; Vestibular Function Tests

Ginger has long been used as an alternative medication to prevent motion sickness. The mechanism of its action, however, is unknown. We hypothesize that ginger ameliorates the nausea associated with motion sickness by preventing the development of gastric dysrhythmias and the elevation of plasma vasopressin. Thirteen volunteers with a history of motion sickness underwent circular vection, during which nausea (scored 0-3, i.e., none to severe), electrogastrographic recordings, and plasma vasopressin levels were assessed with or without ginger pretreatment in a crossover-design, double-blind, randomized placebo-controlled study. Circular vection induced a maximal nausea score of 2.5 +/- 0.2 and increased tachygastric activity and plasma vasopressin. Pretreatment with ginger (1,000 and 2,000 mg) reduced the nausea, tachygastria, and plasma vasopressin. Ginger also prolonged the latency before nausea onset and shortened the recovery time after vection cessation. Intravenous vasopressin infusion at 0.1 and 0.2 U/min induced nausea and increased bradygastric activity; ginger pretreatment (2,000 mg) affected neither. Ginger effectively reduces nausea, tachygastric activity, and vasopressin release induced by circular vection. In this manner, ginger may act as a novel agent in the prevention and treatment of motion sickness.

Topics: Adolescent; Adult; Double-Blind Method; Electrophysiology; Female; Humans; Infusions, Intravenous; Male; Motion; Motion Sickness; Nausea; Phytotherapy; Rotation; Stomach; Vasopressins; Zingiber officinale

An integrated understanding of the physiological mechanisms involved in the genesis of nausea remains lacking. We aimed to describe the psychophysiological changes accompanying visually induced motion sickness, using a motion video, hypothesizing that differences would be evident between subjects who developed nausea in comparison to those who did not. A motion, or a control, stimulus was presented to 98 healthy subjects in a randomized crossover design. Validated questionnaires and a visual analogue scale (VAS) were used for the assessment of anxiety and nausea. Autonomic and electrogastrographic activity were measured at baseline and continuously thereafter. Plasma vasopressin and ghrelin were measured in response to the motion video. Subjects were stratified into quartiles based on VAS nausea scores, with the upper and lower quartiles considered to be nausea sensitive and resistant, respectively. Twenty-eight subjects were exposed to the motion video during functional neuroimaging. During the motion video, nausea-sensitive subjects had lower normogastria/tachygastria ratio and cardiac vagal tone but higher cardiac sympathetic index in comparison to the control video. Furthermore, nausea-sensitive subjects had decreased plasma ghrelin and demonstrated increased activity of the left anterior cingulate cortex. Nausea VAS scores correlated positively with plasma vasopressin and left inferior frontal and middle occipital gyri activity and correlated negatively with plasma ghrelin and brain activity in the right cerebellar tonsil, declive, culmen, lingual gyrus and cuneus. This study demonstrates that the subjective sensation of nausea is associated with objective changes in autonomic, endocrine and brain networks, and thus identifies potential objective biomarkers and targets for therapeutic interventions.

Topics: Adult; Autonomic Nervous System; Case-Control Studies; Cerebral Cortex; Endocrine System; Female; Ghrelin; Humans; Male; Middle Aged; Motion Sickness; Nausea; Vasopressins

This study was to investigate the effect of gastric electrical stimulation (GES) with short pulses, long pulses, short-pulse trains or long-pulse trains on gastric dysrhythmia and motion-sickness signs induced by vasopressin.. Seven male beagle dogs implanted with four pairs of electrodes on gastric serosa were studied. The study was performed in six sessions in a randomized order. In session 1 or 2, either saline or vasopressin was infused without GES. In session 3, 4, 5 and 6, GES with short pulses, long pulses, trains of short pulses or trains of long pulses was performed before and during vasopressin infusion. Gastric slow waves and motion-sickness signs were recorded in each session.. (1) Vasopressin induced gastric dysrhythmia and motion sickness-like signs (ANOVA, P < 0.001). (2) GES with short pulses or trains of short pulses was capable of preventing vasopressin-induced emetic response (P < 0.001), but did not normalize gastric dysrhythmia. (3) GES with long pulses or trains of long pulses was able to normalize gastric dysrhythmia induced by vasopressin (P < 0.001), but showed no effects on vasopressin-induced motion-sickness signs.. GES with short pulses or trains of short pulses prevents vasopressin-induced emetic response with no improvement in gastric dysrhythmia. GES with long pulses or trains of long pulses normalizes gastric dysrhythmia induced by vasopressin with no effects on signs.

Topics: Animals; Dogs; Electric Stimulation Therapy; Gastrointestinal Motility; Male; Motion Sickness; Stomach Diseases; Vasopressins

Gastric electrical stimulation (GES) is known to improve vomiting with short pulses, normalize dysrhythmia with long pulses, and accelerate gastric emptying with 2 channels. The aim of this study was to assess the effects of a new method GES, namely, 2-channel GES with dual pulses on gastric emptying of solids as well as gastric dysrhythmia and emetic responses.. Seven beagle dogs implanted with 4 pairs of electrodes were studied. A novel method of GES was proposed: 2-channel dual-pulse GES in which each stimulus was composed of a short pulse followed with a long pulse, and stimulation was delivered at 2 different locations. The study was performed to test the effects of this new method of GES on vasopressin-induced delayed gastric emptying of solids, gastric dysrhythmia, and emetic responses.. (1) Vasopressin-induced gastric dysrhythmia and emetic responses, as well as delayed gastric emptying of solids (P < .01). (2) Two-channel, but not 1-channel, dual-pulse GES was able to accelerate vasopressin-induced delayed gastric emptying of solids. (3) Both 1- and 2-channel dual-pulse GES was capable of improving dysrhythmia and emetic responses (P < .01).. The novel method of 2-channel dual-pulse GES is capable of accelerating gastric emptying of solids and improving dysrhythmia and emetic responses induced by vasopressin. This new method of GES may have a potential for gastroparesis.

Topics: Animals; Dogs; Electric Stimulation; Female; Gastric Emptying; Motion Sickness; Myoelectric Complex, Migrating; Periodicity; Stomach; Time Factors; Vasopressins; Vomiting

It has been shown that stress changes stimulated pro-inflammatory cytokine production and the sensitivity of stimulated cytokine production to glucocorticoid suppression. While glucocorticoid secretion habituates in response repeated stimulation, it is not known whether stimulation and suppression of cytokine production are also subject to adaptation. Eight healthy young subjects were exposed to repeated nauseogenic body rotation on four consecutive days. On each day subjects were rotated around the vertical axis up to five times for a period of 1 min or until subjects chose to stop due to nausea. Blood and saliva samples were obtained before and after rotation for assessment of cortisol, ACTH, plasma vasopressin (ADH), in vitro TNF-alpha and IL-6 production and glucocorticoid sensitivity of TNF-alpha and IL-6 production. Rotation induced increases of ACTH, cortisol, and ADH in the first session. All endocrine responses habituated over time, except for the free cortisol response in men. Pro-inflammatory cytokine production showed a sex-specific response pattern with increases in men and decreases in women in the first session vs. increases in men and women in the last session. Response patterns of GC sensitivity also changed over time: in the first session, sensitivity increased only in men, but in the last session, GC sensitivity decreased in all subjects. In conclusion, in response to repeated nausea induction, habituation occurs only in the endocrine system and predominantly in women. In the immune system, response patterns change in the favor of inflammatory conditions, with increases in stimulated IL-6 and TNF-alpha and decreases in the effectiveness of glucocorticoid suppression of these cytokines. These presumably unfavorable changes in the inflammatory system are more pronounced men.

Topics: Adaptation, Physiological; Adrenocorticotropic Hormone; Adult; Cytokines; Female; Humans; Hydrocortisone; Interleukin-6; Male; Motion Sickness; Nausea; Reference Values; Rotation; Saliva; Sex Factors; Tumor Necrosis Factor-alpha; Vasopressins

The aim of this study was to investigate the effects of two-channel gastric electrical stimulation (GES) on delayed gastric emptying, gastric dysrhythmias, and motion sickness-like symptoms induced by vasopressin. Seven dogs implanted with four pairs of gastric electrodes and a duodenal cannula were studied in four randomized sessions (saline, vasopressin, single-channel GES, and two-channel GES). The experiment in each session was conducted sequentially as follows: 30-min baseline, ingestion of a liquid meal, 30-min iv infusion of vasopressin or saline, and two 30-min postprandial recordings. In the GES sessions, GES was applied via the first pair of electrodes for single-channel GES or the first and third pairs of electrodes for two-channel GES. Gastric emptying was collected every 15 min via the cannula for a period of 90 min. Results were as follows. (1) Vasopressin induced gastric dysrhythmias, motion sickness-like symptoms, and delayed gastric emptying (P < 0.01, ANOVA). (2) GES normalized gastric dysrhythmias (P < 0.01) but showed no effects on vasopressin-induced emetic response. (3) Two-channel GES improved delayed gastric emptying induced by vasopressin. In comparison with the vasopressin session, two-channel GES, but not single-channel GES, significantly increased gastric emptying at 30 min (43.9+/-12.6 vs. 27.5+/-7.7%; P < 0.03), 60 min (75.3+/-15.1 vs. 54.0+/-17.8%; P < 0.05), and 90 min (91.6+/-9.8 vs. 80.3+/-9.0%; P < 0.05). GES with long pulses is able to normalize gastric dysrhythmias. Two-channel GES improves delayed gastric emptying induced by vasopressin.

Topics: Animals; Dogs; Electric Stimulation Therapy; Gastric Emptying; Male; Motion Sickness; Periodicity; Stomach; Stomach Diseases; Time Factors; Vasopressins

The aim of this study was to investigate the effect of intestinal electrical stimulation on small intestinal dysrhythmia and motion sickness-like symptoms induced by vasopressin. Female dogs chronically implanted with two pairs of electrodes on jejunum serosa were used in a four-session study. Saline and vasopressin were infused in sessions 1 and 2, respectively. Sessions 3 and 4 were the same as session 2, except a long- or short-pulse intestinal electrical stimulation was applied on the proximal pair of electrodes. Intestinal slow waves and motion sickness-like symptoms were recorded in each session. Results were as follows. (1) Vasopressin induced intestinal dysrhythmia, uncoupling of slow waves, and vomiting and motion sickness-like symptoms (P < 0.05, ANOVA). (2) Intestinal electrical stimulation with long pulses, but not short pulses, was capable of preventing vasopressin-induced intestinal dysrhythmia. (3) Intestinal electrical stimulation with short pulses, but not long pulses, prevented vomiting and the motion sickness-like symptoms. It is concluded that vasopressin induces intestinal dysrhythmia. Long-pulse intestinal stimulation normalizes vasopressin-induced intestinal slow-wave abnormalities with no improvement in symptoms. Short-pulse stimulation prevents emetic symptoms induced by vasopressin but has no effect on slow waves. These data suggest different mechanisms involved with different methods of intestinal stimulation.

Topics: Animals; Dogs; Electric Stimulation Therapy; Electrodes, Implanted; Female; Intestinal Diseases; Motion Sickness; Myoelectric Complex, Migrating; Vasoconstrictor Agents; Vasopressins

Recent studies, which have shown an increase of plasma vasopressin (VP) in experimental motion sickness and the efficacy of VP antagonists for motion sickness, suggest an important role of VP in the development of vestibulo-autonomic responses. We have recently found evidence of the co-existence of vasopressinergic neurons with the stress-sensitive chemokinergic neuronal system in the hypothalamo-pituitary pathway in rats, which uses cytokine-induced neutrophil chemoattractant (CINC) as an effector molecule. In this study, to elucidate possible roles of VP and CINC in the vestibulo-autonomic responses, we simultaneously measured plasma VP and CINC concentrations after electrical or caloric vestibular stimulation in urethane-anesthetized rats. Electrical vestibular stimulation with more than 200 microA increased the plasma levels of VP in a current intensity-dependent manner, and stimulation with 500 microA increased the plasma VP levels to 350% of the normal control group, which received no stimulation. Caloric vestibular stimulation with cold water increased the plasma VP levels to 262% of the control group, which received caloric stimulation with water at 37 degrees C, and stimulation with warm water tended to increase the plasma VP levels. Plasma CINC levels were neither affected by electrical nor caloric vestibular stimulation. These findings indicate that vestibular stimulation increased plasma levels of VP but not CINC, and this vestibular-induced activation of VP neurons may be involved in a mechanism of vestibulo-autonomic responses.

Topics: Animals; Autonomic Nervous System; Caloric Tests; Chemokines, CXC; Chemotactic Factors; Electric Stimulation; Growth Substances; Hypothalamo-Hypophyseal System; Intercellular Signaling Peptides and Proteins; Male; Motion Sickness; Rats; Rats, Wistar; Vasopressins; Vestibule, Labyrinth

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 indomethacin. Four 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. Supraphysiological 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.

Topics: Adult; Atropine; Cyclooxygenase Inhibitors; Female; Humans; Indomethacin; Male; Motion Sickness; Nausea; Parasympatholytics; Periodicity; Rotation; Stomach; Vasopressins

The standard human vection model utilized for nausea has been an optokinetic drum. This model may be difficult to extrapolate to the usual clinical setting. Our goals were to develop an experimental model which could induce low grade nausea in humans and to determine the relationship between mild nausea and changes in the electrogastrogram and plasma vasopressin concentrations.. Twenty-one volunteers (11 males, mean age: 37 years) participated. At baseline and throughout the study the electrogastrogram was monitored, blood was drawn for vasopressin assay and symptoms of nausea, dizziness and headache were rated on a 0-10-point scale. Subjects were semireclined in a darkened room while viewing moving bars of light rotating at a rate of 85 degrees s-1. Subjects were asked to rate their proneness to motion sickness and their current level of anxiety at baseline.. Eight subjects developed mild to moderate (mean: 3.6) nausea during vection. Symptoms of nausea were correlated with a reported history of motion sickness (r = 0.49, P < 0.05) but not with anxiety (r = 0.14, P = 0.54). Degrees of nausea correlated with degrees of dizziness (r = 0.47, P < 0.05) but not with headache (r = 0.29, P = 0.14). Subjects who developed mild nausea were not significantly more likely to exhibit altered electrogastrogram or vasopressin than subjects who did not report nausea. Vasopressin levels during baseline and experimental conditions were highly correlated (r = 0.66, P < 0.005 and r = 0.55 P < 0.005, respectively) with reported baseline anxiety.. (1) This new model in humans induced mild nausea that was unrelated to electrogastrogram and vasopressin abnormalities, (2) high correlation between anxiety and vasopressin suggests that vasopressin may not be directly related to nausea, and (3) these data indicate that onset of nausea mediated centrally can occur without associated electrogastrogram changes.

Topics: Adult; Aged; Anxiety; Dizziness; Electromyography; Female; Headache; Humans; Illusions; Male; Middle Aged; Models, Biological; Motion Sickness; Muscle, Smooth; Myoelectric Complex, Migrating; Nausea; Nystagmus, Optokinetic; Reference Values; Regression Analysis; Stomach; Vasopressins

Vasopressin and oxytocin are nonapeptides secreted from the neurohypophysis; increases in vasopressin are associated with nausea and vomiting in some, but not all, species. Our aim was to determine whether plasma vasopressin and oxytocin levels were altered in healthy volunteers who did or did not develop nausea during vection, an optokinetic stimulus which produces the illusion of self-motion. Vection was produced by rotating a drum with an inner surface of black and white vertical stripes around the seated stationary subject. Gastric myoelectrical activity was recorded continuously throughout the experiment with electrodes positioned on the abdominal surface. Plasma samples were obtained before vection and after drum rotation stopped when nausea and tachygastria were present. Vasopressin and oxytocin were extracted from plasma and quantified by RIA. During vection six subjects reported nausea and developed gastric dysrhythmias; six other subjects had no nausea and remained in normal 3-cpm myoelectrical rhythms. Vasopressin and oxytocin values before vection were similar in each group of subjects. One minute after vection stopped, plasma vasopressin levels were significantly greater (P less than 0.05) in subjects experiencing nausea and tachygastrias (35.4 +/- 26.7 pmol/L) than in those without symptoms (2.7 +/- 0.47 pmol/L). Oxytocin levels were unchanged by either vection or nausea. It is concluded that 1) vasopressin, not oxytocin, neurons in the magnocellular-neurohypophyseal system are activated during vection-induced nausea and gastric dysrhythmias; and 2) illusory self-motion may be used safely to study the neuroendocrine responses to brain-gut interactions and nausea in man.

Topics: Adult; Brain; Digestive System Physiological Phenomena; Female; Humans; Male; Motion Sickness; Nausea; Ovum; Oxytocin; Vasopressins

Experiments performed on Space Shuttle flights have emphasized study of the earliest effects of the cephalad fluid shift resulting from microgravity. Analysis of one subject's urine collected during flight showed that a sharp increase in antidiuretic hormone occurred within 2 h of launch, followed by an increase in cortisol excretion. Although this subject had symptoms of the space adaptation syndrome (SAS), inflight data from Spacelab missions suggested that these transient changes were not caused by SAS. Unpaired t-tests and Mann-Whitney tests showed that before and after flight, plasma thyroxine and urine osmolality were significantly higher in Shuttle crewmembers who exhibited more severe symptoms of SAS than in asymptomatic crewmembers. Collection of inflight data from more crewmembers should allow distinction between the effects of SAS and effects of weightlessness, and in the future several additional fluid regulation hormones will be measured in samples from crewmembers for a more complete understanding of fluid control during weightlessness.

Topics: Adaptation, Physiological; Aldosterone; Body Fluids; Humans; Hydrocortisone; Motion Sickness; Osmolar Concentration; Space Flight; Thyroxine; Vasopressins; Water-Electrolyte Balance; Weightlessness

The stress of motion sickness was experimentally provoked by Coriolis effect. Significant and reproducible increases from the basal serum level (delta mean +/- S.E.) of antidiuretic hormone delta - ADH: 48.2 +/- 4.6 pg/ml; p less than 0.0005), of growth hormone (delta - hGH: 10.0 +/- 1.2 ng/ml; p less than 0.0005), of prolactin (delta - hPRL: 186.5 +/- 29.9 muU/ml; p less than 0.0005), and of cortisol (delta - F; 12.3 +/- 0.9 microgram%; p less than 0.0005) were observed, whereas the luteinizing hormone levels did not change significantly. The stimulation of hormone secretion induced by different degrees of motion sickness seems to correlate with the severity of motion sickness. The secretion of antidiuretic hormones is the most sensitive indicator for the stress of motion sickness whereas growth hormone, prolactin, and cortisol responses to the stress of motion sickness are more delayed and less pronounced.

Topics: Blood Glucose; Growth Hormone; Humans; Hydrocortisone; Male; Motion Sickness; Osmolar Concentration; Prolactin; Vasopressins