vasoactive-intestinal-peptide and Nausea

Topics: Adenosine Triphosphate; Animals; Autonomic Nervous System; Electric Stimulation; Gastric Emptying; Humans; Muscle, Smooth; Nausea; Neurotransmitter Agents; Stomach; Vagotomy; Vagus Nerve; Vasoactive Intestinal Peptide; Vomiting

Impaired gastric slow waves, frequent gastrointestinal (GI) symptoms and altered GI peptides have been reported in Scleroderma (SSc) patients. The aim of this study was to investigate the associations among these three important components in GI dysmotility. Seventeen fasted SSc patients underwent four channel surface electrogastrography, measuring % of normal gastric slow waves or dysrhythmia. Patients completed a questionnaire designed by us to assess demographics, upper and lower GI symptoms (symptom presence, frequency and impact on quality of life, QOL), by YES/NO, Likert Scales and Visual Analogue Scales 1-100 mm (called GI Dysmotility Questionnaire, GIDQ) and health-related QOL by SF-36. Fasting plasma vasoactive intestinal peptide (VIP) and motilin levels were measured by peptide immunoassays. There were significant correlations between percentages of gastric dysrhythmias (bradygastria or arrhythmia) and a number of major GI symptoms such as nausea, abdominal bloating and pain. The plasma level of VIP was correlated positively with % dysrhythmia but negatively with % normal slow waves. Motilin was positively correlated with slow wave coupling (coordination). No major differences were noted in the measured peptides or gastric slow waves between limited SSc and diffuse SSc. Correlations were noted between SF-36 domain scores and our GIDQ scores. In SSc patients, gastric dysrhythmias are correlated with certain GI symptoms. Correlations are also noted between plasma VIP/Motilin levels and gastric slow waves. Thus in SSc, gastric dysrhythmias may be predictive of development of certain dyspeptic symptoms. Plasma VIP may be involved in the development of dysrhythmias.

Topics: Adult; Disease Progression; Electromyography; Electrophysiology; Female; Gastrointestinal Diseases; Humans; Male; Middle Aged; Motilin; Nausea; Peptides; Scleroderma, Systemic; Skin; Stomach; Surveys and Questionnaires; Vasoactive Intestinal Peptide

Based on studies in animals and humans, it has been suggested that nausea activates the hypothalamo-neurohypophyseal system with resultant increases in circulating concentrations of oxytocin or vasopressin. The purpose of these studies was to determine in humans whether nausea is associated with increases in circulating concentrations of neurohypophyseal hormones or various enteropancreatic peptides (vasoactive intestinal polypeptide, substance P, or pancreatic polypeptide). Nausea, induced by intravenous infusion of apomorphine, was associated with fivefold to 75-fold increases in plasma vasopressin concentrations in 7 subjects (mean increase, 41-fold), with no change in plasma oxytocin levels. Furthermore, nausea was associated with sevenfold to 16-fold increases in plasma pancreatic polypeptide concentrations (mean increase, ninefold), with no change in plasma levels of vasoactive intestinal polypeptide or substance P. In 1 subject refractory to nausea, there was no increase in plasma vasopressin or pancreatic polypeptide concentrations with apomorphine. These studies indicate that nausea in humans is associated with vasopressin and pancreatic polypeptide release.

Topics: Adult; Apomorphine; Female; Humans; Infusions, Intravenous; Nausea; Oxytocin; Pancreatic Polypeptide; Substance P; Vasoactive Intestinal Peptide; Vasopressins