Department of Anesthesiology and Intensive Care, Örebro University Hospital, Örebro, Sweden.
Acta Anaesthesiol Scand. 2013 Sep;57(8):1002-9. doi: 10.1111/aas.12134. Epub 2013 May 29.
A recent study demonstrated that reflux is associated with impaired pressure augmentation in the esophagogastric junction (EGJ), caused by diaphragmal contractions during inspiration. It is unknown whether this augmentation is influenced by opioids. Swallowing difficulties can be a poorly recognised side effect of remifentanil. Here, we investigated whether remifentanil influences inspiratory EGJ augmentation and evaluated subjective swallowing difficulties induced by remifentanil. We also used the peripheral opioid receptor antagonist methylnaltrexone to evaluate whether these effects are centrally or peripherally mediated.
Ten healthy volunteers participated in a double-blind, randomised, 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 methylnaltrexone 0.15 mg/kg or saline subcutaneously 30 min before the target-controlled infusion of remifentanil of 3 ng/mL. EGJ pressures were measured by high-resolution manometry. Swallowing difficulties were assessed when volunteers performed dry swallows. The outcomes were the differences in EGJ pressures at baseline and during remifentanil infusion and with methylnaltrexone vs. placebo. Differences in swallowing difficulties before and during remifentanil, and with methylnaltrexone vs. placebo were also recorded.
Remifentanil decreased the inspiratory EGJ augmentation and induced swallowing difficulties. No statistically significant differences between methylnaltrexone and placebo occasions were found.
Remifentanil may increase risk for gastroesophageal reflux by decreasing the inspiratory EGJ augmentation. The clinical significance of remifentanil-induced swallowing difficulties is to be studied further. Given the limited sample size, it cannot be concluded whether these effects are centrally or peripherally mediated.
最近的一项研究表明，反流与膈收缩引起的食管胃结合部（EGJ）压力增强受损有关，这种增强是在吸气时发生的。目前尚不清楚这种增强是否受阿片类药物的影响。吞咽困难可能是瑞芬太尼的一种被低估的不良反应。在这里，我们研究了瑞芬太尼是否会影响吸气时 EGJ 增强，并评估了瑞芬太尼引起的主观吞咽困难。我们还使用外周阿片受体拮抗剂甲基纳曲酮来评估这些作用是中枢还是外周介导的。
10 名健康志愿者在瑞典厄勒布鲁大学医院参加了一项双盲、随机、交叉试验。他们在两次不同的时间点接受研究，在这两次时间点，他们被随机分配在皮下接受 0.15mg/kg 的甲基纳曲酮或生理盐水，在这之后 30 分钟内接受瑞芬太尼目标控制输注 3ng/ml。EGJ 压力通过高分辨率测压法进行测量。志愿者进行干吞咽时评估吞咽困难。研究结果为基础状态和瑞芬太尼输注期间以及与甲基纳曲酮和安慰剂相比时 EGJ 压力的差异。还记录了在瑞芬太尼之前和期间以及与甲基纳曲酮和安慰剂相比时吞咽困难的差异。
瑞芬太尼降低了吸气时的 EGJ 增强，并引起了吞咽困难。在甲基纳曲酮和安慰剂的情况下，没有发现统计学上的显著差异。
瑞芬太尼可能通过降低吸气时的 EGJ 增强而增加胃食管反流的风险。瑞芬太尼引起的吞咽困难的临床意义有待进一步研究。鉴于样本量有限，无法得出这些作用是中枢还是外周介导的结论。
