Savilampi J, Magnuson A, Ahlstrand R
Department of Anesthesiology and Intensive Care, Örebro University Hospital, Örebro, Sweden.
Acta Anaesthesiol Scand. 2015 Oct;59(9):1126-36. doi: 10.1111/aas.12534. Epub 2015 Apr 29.
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.
最近的研究表明,瑞芬太尼会增加误吸风险并导致主观吞咽困难。其机制尚未完全明确。在此,我们研究了瑞芬太尼是否会损害食管动力,并推测这可能是一个潜在机制。使用纳洛酮来评估瑞芬太尼的作用是否通过阿片受体介导。我们还研究了主观吞咽困难以及甲氧氯普胺对瑞芬太尼诱导效应的影响。
14名健康志愿者参与了瑞典厄勒布鲁大学医院的一项双盲、随机、交叉试验。他们在两个不同的时间段接受研究,在此期间,他们被随机分配在靶控输注瑞芬太尼(三个靶位浓度:1、2和3 ng/ml)前5分钟接受6 μg/kg静脉推注后以0.1 μg/kg/分钟输注的纳洛酮,或生理盐水。在两个时间段,最终测量前均给予0.2 mg/kg甲氧氯普胺。在每个测量条件下进行5次吞咽,通过高分辨率测压法测量定义食管动力的指标。观察指标为基线与瑞芬太尼输注期间、纳洛酮与安慰剂、甲氧氯普胺给药前后瑞芬太尼作用下指标的差异。还记录了吞咽困难的差异。
瑞芬太尼降低了吞咽诱发的食管胃交界区松弛和食管蠕动的延迟时间。纳洛酮或甲氧氯普胺对瑞芬太尼诱导的效应无显著影响,且我们未检测到吞咽困难方面的差异。
瑞芬太尼可诱发食管动力功能障碍;这可能导致反流和误吸风险升高。