Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic idiopathic gastric stasis can be responsible for unexplained dyspepsia. Because exogenous opiates inhibit gastric emptying and endogenouslike substances are present in the gastrointestinal tract, we tested the hypothesis that increased endogenous opiate activity may be responsible for chronic idiopathic gastric stasis. Eighteen patients with chronic idiopathic gastric stasis and ten healthy volunteers were studied by gastrointestinal manometry. Scintigraphic technique also was used, during which either intravenous saline or naloxone hydrochloride were infused. Manometry showed gastric hypomotility in ten patients and duodenal hyperdyskinesia in the remaining eight patients. Naloxone did not alter gastric emptying in healthy subjects or corrected gastric stasis in patients with gastric hypomotility, while it normalized gastric emptying in patients with duodenal dyskinesia. It seems that either gastroparesis or duodenal dyskinesia can promote gastric stasis and chronic dyspepsia, and endogenous opiates participate in the pathogenesis of gastric stasis in patients with duodenal dyskinesia.
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PMID:Functional dyspepsia and chronic idiopathic gastric stasis. Role of endogenous opiates. 396 53

Endogenous opioids have been implicated not only in the process of feeding but also in the control of gastric sensitivity and gastric motor responses, and impairment of antinociceptive opioid pathways has been hypothesized to contribute to the pathogenesis of functional dyspepsia. Our aim was to study the effect of suppression of endogenous opioid action by naloxone on gastric sensorimotor function in healthy volunteers. During intravenous administration of saline or naloxone (0.4 mg intravenous bolus followed by continuous infusion 20 microg kg(-1) h(-1)), sensitivity to gastric distension, gastric accommodation and fundic phasic contractility were evaluated by barostat in 15 subjects. Nutrient tolerance and meal-related symptoms were assessed using a satiety drinking test (n = 13), and solid and liquid gastric emptying were evaluated by breath test (n = 14). Naloxone did not influence gastric compliance and sensitivity. No effect on preprandial gastric tone was found but meal-induced accommodation was significantly inhibited by naloxone (P = 0.031). Subjects receiving naloxone demonstrated a higher motility index before (20.8 +/- 2.4 vs 28.0 +/- 1.9 mL s(-1), P = 0.007) and after (15.2 +/- 2.0 vs 22.7 +/- 1.5 mL s(-1), P = 0.0006) the meal. Naloxone significantly decreased the amount of food ingested at maximum satiety (715.4 +/- 77.7 vs 617.3 +/- 61.3 mL, P = 0.03). No effect of naloxone on gastric emptying was observed and intensity of postprandial symptoms was unchanged. These observations suggest that endogenous opioids are involved in the control of gastric accommodation and phasic contractility but not in the control of sensitivity to gastric distension or gastric emptying in healthy volunteers.
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PMID:Role of endogenous opioids in the control of gastric sensorimotor function. 1848 49

This study investigated whether the curative effect of short-pulse gastric electrical stimulation (GES) on the vasopressin-induced dyspeptic symptoms was mediated by central opioid peptide-producing neurons. Five female beagle dogs implanted with 1 pair of electrodes in gastric serosa were used in a two-experiment study. In experiment one, the brain was scanned by positron emission tomography in 3 dogs with and without short-pulse GES, and the radioactivity in nuclei of solitary tract (NST) and hypothalamus was detected. Experiment two was composed of 4 sessions. In session one, the dogs were injected with vasopressin in the absence of short-pulse GES. With session two, the short-pulse GES was simultaneously given via the electrodes with the injection of vasopressin. In sessions three and four, naloxone and naloxone methiodide was administered respectively in the presence of short-pulse GES. Motion sickness-like symptoms were scored and compared among the different sessions. The results showed that the short-pulse GES significantly increased the radioactivity in NST and hypothalamic nuclei (P<0.05, vs control). The short-pulse GES could ameliorate the vasopressin-induced motion sickness-like symptoms in dogs. Naloxone, but not naloxone methiodide could attenuate the curative effects of short-pulse GES. It is concluded that NST and hypothalamic nuclei may participate in the mediation of the curative effects of short-pulse GES on dyspepsia-like symptoms. Central opioid peptide-containing neurons presumably mediate the therapeutic effect on dyspeptic symptoms of short-pulse GES.
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PMID:Central opioid peptide-containing neurons mediates therapeutic effect of short-pulse gastric electrical stimulation on dyspepsia-like symptoms in dogs. 2003 10