Geeraerts B, Mimidis K, van Oudenhove L, Vos R, Karamanolis G, Tack J
Division of Gastroenterology, Department of Pathophysiology, University Hospital Gasthuisberg, KU Leuven, Belgium.
Neurogastroenterol Motil. 2008 Oct;20(10):1094-102. doi: 10.1111/j.1365-2982.2008.01144.x. Epub 2008 May 15.
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.
内源性阿片类物质不仅与进食过程有关，还与胃敏感性和胃运动反应的控制有关，并且抗伤害感受性阿片通路的损害被认为与功能性消化不良的发病机制有关。我们的目的是研究纳洛酮抑制内源性阿片作用对健康志愿者胃感觉运动功能的影响。在静脉注射生理盐水或纳洛酮（0.4mg静脉推注，随后以20μg·kg⁻¹·h⁻¹持续输注）期间，通过压力传感器对15名受试者的胃扩张敏感性、胃容纳功能和胃底相性收缩进行评估。使用饱腹感饮水试验评估营养耐受性和进餐相关症状（n = 13），并通过呼气试验评估固体和液体胃排空（n = 14）。纳洛酮不影响胃顺应性和敏感性。未发现对餐前胃张力有影响，但纳洛酮显著抑制进餐诱导的胃容纳功能（P = 0.031）。接受纳洛酮的受试者在进餐前（20.8±2.4 vs 28.0±1.9 mL·s⁻¹，P = 0.007）和进餐后（15.2±2.0 vs 22.7±1.5 mL·s⁻¹，P = 0.0006）的运动指数较高。纳洛酮显著降低最大饱腹感时摄入的食物量（715.4±77.7 vs 617.3±61.3 mL，P = 0.03）。未观察到纳洛酮对胃排空有影响，餐后症状强度未改变。这些观察结果表明，内源性阿片类物质参与胃容纳功能和相性收缩的控制，但不参与健康志愿者对胃扩张敏感性或胃排空的控制。
