贲门失弛缓症患者的膈肌电图(DEMG)。

H Ujiie, M Hongo, Y Okuno, M Yamada, T Toyota
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引用次数: 1

摘要

膈肌收缩后LES压力增加是胃食管反流的屏障机制之一。在贲门失弛缓症患者中,湿吞咽后不完全的LES松弛是血压测量的特征之一,同时伴有蠕动丧失。另一方面,有报道称吞咽用力或食管扩张对膈肌收缩引起的LES压力升高没有影响,这种情况与贲门失弛缓症相似。因此,为了评估膈肌收缩是否与贲门失弛缓症的病因有关,我们使用双极电极记录了12例贲门失弛缓症患者和4例正常人的膈肌电图(DEMG)。正常人和贲门失弛缓症患者的分相DEMG波幅为80 ~ 90微伏。直腿抬高(SLR)和腹胀(AD)两种动作均引起膈肌收缩,正常受试者和贲门失弛缓症患者的LES压和DEMG振幅均升高。从该设备获得的数据,我们得出结论,膈肌受累不太可能是贲门失弛缓症患者LES功能障碍的发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Diaphragmatic electromyography (DEMG) in achalasia patients].

LES pressure increase following diaphragmatic contraction as a pinch-cock action acts as one of the barrier mechanism for gastroesophageal reflux. In achalasia patients, incomplete LES relaxation following wet swallow is one of the characteristic manometric findings, along with loss of peristalsis. On the other hand, it has been reported that swallowing effort or esophageal distention have no effect on the increase of LES pressure induced by diaphragmatic contraction, which condition is similar to achalasia. Therefore, to evaluate that whether diaphragmatic contraction is involved in the cause of achalasia, we recorded diaphragmatic electromyography (DEMG) using bipolar electrodes in 12 achalasia patients and 4 normal subjects. The phasic DEMG amplitude was 80-90 microV in normal subjects and achalasia patients. LES pressure and DEMG amplitude increased during both straight leg raising (SLR) and abdominal distention (AD), both of the maneuver induce diaphragmatic contraction, in normal subjects and achalasia patients similarly. From the data obtained with this equipment, we conclude that diaphragmatic involvement is not likely as a pathogenesis of LES dysfunction in achalasia patients.

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