Schoeman M N, Holloway R H
Department of Gastroenterology, Royal Adelaide Hospital, South Australia.
Gut. 1994 Feb;35(2):152-8. doi: 10.1136/gut.35.2.152.
The study evaluates the triggering and characteristics of secondary oesophageal peristalsis in 25 healthy volunteers. Secondary peristalsis was stimulated by rapid intraoesophageal injection of boluses of air and water, and by a five second oesophageal distension with a balloon. Air and water boluses triggered secondary peristalsis that started in the proximal oesophagus regardless of injection site. Response rates were volume dependent with 83% of the 20 ml air boluses triggering secondary peristalsis compared with 2% for the 2 ml water bolus (p < 0.0001). Response rates for air and water were similar for equal bolus volumes and were not influenced by the site of injection. In contrast, balloon distension usually induced a synchronous contraction above the balloon, with secondary peristalsis starting below the balloon after deflation. The peristaltic response rate to balloon distension was also volume dependent and the middle balloon was more effective in triggering secondary peristalsis than either the upper or lower balloons (p < 0.001). Secondary peristaltic amplitude was less than that of primary peristalsis (p < 0.001). Secondary peristaltic velocity with a water bolus was slower (p = 0.001) than that of primary peristalsis. Intravenous atropine significantly reduced secondary peristaltic responses to all stimuli. There was also a significant reduction in pressure wave amplitude for air stimulated secondary peristalsis while those for the water responses were similar. Secondary peristaltic velocity with air and water boluses was not changed by atropine. The reproducibility of testing secondary peristalsis was examined six volunteers and did not show any significant differences on separate test days in response rate and peristaltic amplitude or velocity. It is concluded that in normal subjects, secondary peristalsis can be more reliably triggered by intraoesophageal air or water infusion than balloon distension. Secondary peristaltic amplitude and velocity are stimulus but not site or volume dependent and propagation is partially mediated by cholinergic nerves.
该研究评估了25名健康志愿者食管继发性蠕动的触发因素和特征。通过向食管内快速注射空气团和水团,以及用气囊对食管进行5秒钟的扩张来刺激继发性蠕动。空气团和水团触发的继发性蠕动始于食管近端,与注射部位无关。反应率与注入量有关,20毫升空气团触发继发性蠕动的比例为83%,而2毫升水团的这一比例为2%(p<0.0001)。等量的空气团和水团的反应率相似,且不受注射部位的影响。相比之下,气囊扩张通常会在气囊上方诱发同步收缩,放气后继发性蠕动在气囊下方开始。对气囊扩张的蠕动反应率也与注入量有关,中间的气囊比上部或下部气囊更有效地触发继发性蠕动(p<0.001)。继发性蠕动幅度小于原发性蠕动(p<0.001)。水团引发的继发性蠕动速度比原发性蠕动慢(p=0.001)。静脉注射阿托品显著降低了对所有刺激的继发性蠕动反应。空气刺激引发的继发性蠕动的压力波幅度也显著降低,而水刺激引发的继发性蠕动的压力波幅度相似。阿托品未改变空气团和水团引发的继发性蠕动速度。对6名志愿者进行了继发性蠕动测试的可重复性检查,在不同测试日的反应率、蠕动幅度或速度方面未显示出任何显著差异。得出的结论是,在正常受试者中,通过向食管内注入空气或水比气囊扩张能更可靠地触发继发性蠕动。继发性蠕动幅度和速度取决于刺激因素,而非部位或注入量,其传播部分由胆碱能神经介导。