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Recent studies have shown that remifentanil increases the risk of aspiration and induces subjective swallowing difficulties. The mechanisms are not completely understood. Here, we investigated whether remifentanil impairs esophageal motility and hypothesized that this is one possible underlying mechanism. Naloxone was used to evaluate whether the effects of remifentanil are mediated through opioid receptors. We also examined subjective swallowing difficulties and the influence of metoclopramide on remifentanil-induced effects.Fourteen healthy volunteers participated in a double-blind, randomized, cross-over trial at the University Hospital in Örebro, Sweden. They were studied on two different occasions, during which they were randomly assigned to receive either naloxone given as a bolus of 6 μg/kg followed by an infusion of 0.1 μg/kg/min, or saline 5 min before target-controlled infusions of remifentanil at three target-site concentrations: 1, 2, and 3 ng/ml. On both occasions, 0.2 mg/kg metoclopramide was given before the final measurement. Five swallows were performed during each measuring condition, and the metrics defining esophageal motility were measured by high-resolution manometry. Outcomes were differences in the metrics at baseline vs. during remifentanil infusion, with naloxone vs. placebo, and with remifentanil before and after metoclopramide administration. Differences in swallowing difficulties were also recorded.Remifentanil decreased swallow-evoked esophagogastric junction relaxation and the latency time of esophageal peristalsis. There were no significant effects of naloxone or metoclopramide on remifentanil-induced effects, and we detected no differences in swallowing difficulties.Remifentanil induces dysfunction of esophageal motility; this may contribute to the elevated risk of regurgitation and aspiration.