naloxone and Dyspepsia

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.

Topics: Adult; Chronic Disease; Duodenum; Dyspepsia; Endorphins; Female; Gastric Emptying; Gastrointestinal Motility; Humans; Male; Manometry; Middle Aged; Naloxone; Time Factors

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.

Topics: Adult; Breath Tests; Drinking; Dyspepsia; Eating; Female; Food; Gastrointestinal Motility; Humans; Naloxone; Opioid Peptides; Postprandial Period; Satiation; Stomach

Non-ulcer dyspepsia (NUD) is one of the core functional bowel disorders. There has been recent emphasis on possible abnormal brain-gut interactions as being central to its pathophysiology. In this preliminary study, we examined central opioid tone in Helicobacter pylori-negative NUD patients using naloxone, an opioid antagonist, which stimulates pituitary-adrenal activity. The opioid system is known to govern nociceptive processing and to play a role in gut motor activity.. Eight subjects with NUD and 8 age- and sex-matched healthy subjects were examined.. Naloxone, 0.125 mg/kg, was administered at time 0. Adrenocorticotropin (ACTH) and cortisol responses were measured over a 120-min period. Maximum pituitary-adrenal responses in the 2 groups were compared.. The ACTH response was significantly attenuated in the NUD group (p < 0.05). The cortisol response did not differ between the 2 groups (p = 0.7).. Central opioid tone may be reduced in subjects with NUD. Our preliminary findings suggest that altered opioidergic activity may contribute to NUD pathophysiology, influencing the symptom profile through altered gut motor activity or possibly by influencing visceral sensitivity.

Topics: Adrenocorticotropic Hormone; Adult; Case-Control Studies; Dyspepsia; Female; Humans; Hydrocortisone; Male; Naloxone; Narcotic Antagonists; Pituitary-Adrenal System