Coulie B, Tack J, Peeters T, Janssens J
Department of Internal Medicine, University Hospital Gasthuisberg, Catholic University of Leuven, Belgium.
Gut. 1998 Sep;43(3):395-400. doi: 10.1136/gut.43.3.395.
During the interdigestive state in humans, erythromycin 40 mg induces a premature activity front that starts in the stomach, while erythromycin 200 mg induces a prolonged period of enhanced antral contractile activity.
To study the involvement of a cholinergic pathway in the motor effects of erythromycin using the muscarinic antagonist atropine and the neural 5-HT1 receptor agonist sumatriptan.
In 30 healthy volunteers, fasted antroduodenojejunal motor activity was studied by stationary manometry. Placebo (n = 10), atropine (15 micrograms/kg intravenous bolus plus 15 micrograms/kg/h over 30 minutes; n = 10), or sumatriptan (6 mg subcutaneously; n = 10) was administered, followed by infusion of erythromycin 40 mg or 200 mg.
After placebo, erythromycin 40 mg induced a premature activity front with gastric onset after 19.1 (1.7) minutes in all volunteers. After atropine, erythromycin 40 mg failed to induce a premature activity front during a 60 minute period in all volunteers (p < 0.001), while sumatriptan prevented the induction of a premature activity front during a 60 minute period in all but one volunteer (p < 0.005). The number of antral contractions and their mean amplitude in the 60 minutes after erythromycin 200 mg did not differ significantly after atropine or sumatriptan versus placebo.
The antral motor effects of erythromycin in humans are mediated via different pathways. The induction of a premature activity front is mediated through activation of an intrinsic cholinergic pathway, while the induction of enhanced antral contractile activity may be mediated via a pathway potentially involving activation of a muscular receptor.
在人类消化间期，40毫克红霉素可诱发始于胃部的过早活动波峰，而200毫克红霉素则可诱发胃窦收缩活动增强的持续期。
使用毒蕈碱拮抗剂阿托品和神经5-羟色胺1（5-HT1）受体激动剂舒马曲坦，研究胆碱能途径在红霉素运动效应中的作用。
对30名健康志愿者采用固定测压法研究空腹状态下胃窦十二指肠空肠的运动活性。分别给予安慰剂（n = 10）、阿托品（静脉推注15微克/千克，随后30分钟内以15微克/千克/小时的速度输注；n = 10）或舒马曲坦（皮下注射6毫克；n = 10），之后输注40毫克或200毫克红霉素。
给予安慰剂后，40毫克红霉素在所有志愿者中于19.1（1.7）分钟后诱发了始于胃部的过早活动波峰。给予阿托品后，40毫克红霉素在所有志愿者中60分钟内均未诱发过早活动波峰（p < 0.001），而给予舒马曲坦后，除一名志愿者外，其他所有志愿者在60分钟内均未诱发过早活动波峰（p < 0.005）。给予200毫克红霉素后60分钟内，阿托品或舒马曲坦组的胃窦收缩次数及其平均振幅与安慰剂组相比无显著差异。
红霉素对人类胃窦部的运动效应通过不同途径介导。过早活动波峰的诱发是通过激活内在胆碱能途径介导的，而胃窦收缩活动增强的诱发可能是通过一条可能涉及肌肉受体激活的途径介导的。
