Salem M Ramez, Bruninga Keith W, Dodlapatii Jyothi, Joseph Ninos J
Department of Anesthesiology and Internal Medicine, Section of Gastroenterology, Advocate Illinois Masonic Medical Center, Chicago, IL 60657, USA.
Anesthesiology. 2008 Nov;109(5):806-10. doi: 10.1097/ALN.0b013e31818a37dc.
The authors examined the influence of metoclopramide on cricoid pressure-induced relaxation of the lower esophageal sphincter (LES) in awake human volunteers.
With local institutional review board approval, measurements of LES and intragastric pressures were made in 10 consenting volunteers before cricoid pressure application, during 15 s of cricoid pressure application, and after release of cricoid pressure. The measurements were repeated after 0.15 mg/kg intravenous metoclopramide. Cricoid pressure was applied by one investigator trained to consistently apply a force of 44 N.
Cricoid pressure resulted in immediate decrease in LES and barrier pressures from 14.1 +/- 2.9 mmHg to 3.2 +/- 3.7 mmHg and from 9.6 +/- 3.4 mmHg to -1.8 +/- 2.9 mmHg, respectively. These pressures promptly returned to baseline values after release of cricoid pressure. LES and barrier pressures increased after metoclopramide from 14.5 +/- 3.1 to 19.6 +/- 4.7 mmHg and from 10.2 +/- 3.6 to 14.1 +/- 5.5 mmHg, respectively. Cricoid pressure applied after metoclopramide resulted in immediate decreases in LES and barrier pressures to levels comparable to cricoid pressure before metoclopramide, but immediately returned to precricoid values after release of pressure.
The current investigation demonstrates that cricoid pressure reflexly decreases LES tone and barrier pressure in awake subjects. Although metoclopramide increased LES and barrier pressures, it did not attenuate cricoid pressure-induced relaxation of the LES and barrier pressures and thus seems to have no value in preventing gastroesophageal reflux during cricoid pressure. Metoclopramide may be useful in preventing reflux when there is need to release or discontinue cricoid pressure.
作者研究了甲氧氯普胺对清醒人类志愿者中环状软骨压迫引起的食管下括约肌（LES）松弛的影响。
经当地机构审查委员会批准，在10名同意参与的志愿者身上测量LES和胃内压力，分别在施加环状软骨压迫前、施加环状软骨压迫15秒期间以及解除环状软骨压迫后进行测量。在静脉注射0.15mg/kg甲氧氯普胺后重复测量。环状软骨压迫由一名经过培训的研究人员施加，该人员始终施加44N的力。
环状软骨压迫导致LES压力和屏障压力立即下降，分别从14.1±2.9mmHg降至3.2±3.7mmHg，从9.6±3.4mmHg降至-1.8±2.9mmHg。解除环状软骨压迫后，这些压力迅速恢复到基线值。甲氧氯普胺给药后，LES压力和屏障压力分别从14.5±3.1mmHg增加到19.6±4.7mmHg，从10.2±3.6mmHg增加到14.1±5.5mmHg。甲氧氯普胺给药后施加环状软骨压迫导致LES压力和屏障压力立即下降至与给药前环状软骨压迫时相当的水平，但压力解除后立即恢复到压迫前的值。
当前研究表明，环状软骨压迫可反射性降低清醒受试者的LES张力和屏障压力。尽管甲氧氯普胺增加了LES压力和屏障压力，但它并未减弱环状软骨压迫引起的LES和屏障压力的松弛，因此在环状软骨压迫期间预防胃食管反流似乎没有价值。当需要解除或停止环状软骨压迫时，甲氧氯普胺可能有助于预防反流。
