Barthet M, Bouvier M, Pecout C, Berdah S, Viviand X, Mambrini P, Abou E, Salducci J, Grimaud J C
Department of Gastroenterology, Hopital Nord, Marseille, France.
Aliment Pharmacol Ther. 1998 Jul;12(7):647-52. doi: 10.1046/j.1365-2036.1998.00346.x.
Trimebutine is an opiate modulator of the gastrointestinal motility that interacts with enkephalinergic receptors.
To evaluate the effects of trimebutine (50 mg intravenous injection) on the motility of the sphincter of Oddi (SO) as assessed by endoscopic manometry.
Endoscopic manometry was performed on 15 cholecystectomized patients who presented with symptoms suggestive of SO dysfunction. Prior to the endoscopic manometry, endoscopic ultrasonography was performed in order to rule out the possible presence of a bile duct stone.
Injecting trimebutine resulted in a significant increase in the SO antegrade phasic contraction rate (P = 0.02). Trimebutine decreased the basal pressure of the SO (32.5 vs. 27.5 mmHg), but the difference is not statistically significant (P = 0.11). The effects of trimebutine differed depending on the basal SO motility anomalies involved, but the period of latency was similar (mean 89 s: range 30-240 s). The basal anomalies were an increased basal SO pressure of > 40 mmHg in three patients, a tachyoddia (frequency of phasic contractions (PC) > 10/min) in six patients, prolonged PC (> 10 s) in two patients and an absence of phasic contraction in one patient. The basal pressure of the SO decreased in the three patients presenting with SO hyperpressure, but returned to a normal value in one case. The frequency of the PC decreased to normal in three out of the six patients with tachyoddia. The duration of the PC returned to normal in the two patients with prolonged PC whereas their frequencies increased. Prolonged PC developed in the patient without any detectable phasic contraction.
Trimebutine modulates SO motility in various ways depending on the basal SO motility anomaly observed after cholecystectomy. This regulatory effect suggests the existence of encephalinergic control of SO motility.
曲美布汀是一种与脑啡肽能受体相互作用的胃肠道动力阿片类调节剂。
通过内镜测压评估曲美布汀（50mg静脉注射）对Oddi括约肌（SO）动力的影响。
对15例有SO功能障碍症状的胆囊切除患者进行内镜测压。在内镜测压前，进行内镜超声检查以排除胆管结石的可能存在。
注射曲美布汀导致SO顺行性相性收缩率显著增加（P = 0.02）。曲美布汀降低了SO的基础压力（32.5对27.5mmHg），但差异无统计学意义（P = 0.11）。曲美布汀的作用因所涉及的基础SO动力异常而异，但潜伏期相似（平均89秒：范围30 - 240秒）。基础异常包括3例患者SO基础压力> 40mmHg升高，6例患者心动过速（相性收缩（PC）频率> 10次/分钟），2例患者PC延长（> 10秒），1例患者无相性收缩。3例SO高压患者的SO基础压力降低，但1例恢复到正常值。6例心动过速患者中有3例PC频率降至正常。2例PC延长患者的PC持续时间恢复正常，而频率增加。在无任何可检测到的相性收缩的患者中出现了PC延长。
根据胆囊切除术后观察到的基础SO动力异常，曲美布汀以多种方式调节SO动力。这种调节作用提示存在对SO动力的脑啡肽能控制。
