Holloway R H, Dodds W J, Helm J F, Hogan W J, Dent J, Arndorfer R C
Gastroenterology. 1986 Apr;90(4):924-9. doi: 10.1016/0016-5085(86)90869-3.
The human lower esophageal sphincter (LES) is believed to be innervated by nonadrenergic, noncholinergic inhibitory nerves, and cholinergic excitatory nerves. In idiopathic achalasia, LES relaxation is abnormal because the inhibitory nerves to the sphincter are either absent or functionally impaired. The integrity of cholinergic excitatory nerves to the LES, however, has not been thoroughly evaluated. In 27 patients with untreated idiopathic achalasia, and 21 healthy volunteers, we investigated the hypothesis that postganglionic cholinergic nerves to the LES are functionally intact in achalasia. The LES responses to atropine, edrophonium, methacholine, amyl nitrite, and pentagastrin were assessed. In 2 achalasia patients, patterns of fasting motor activity in the LES were investigated during overnight manometric studies. Resting LES pressure was significantly greater in the achalasia patients, 41 +/- 4 mmHg (mean +/- SE), than in the normal subjects, 20 +/- 2 mmHg. Atropine significantly reduced LES pressure in both groups by 30%-75%. Edrophonium increased LES pressure in the achalasia patients but had negligible effect on the normal subjects. The LES in achalasia patients exhibited an increased sensitivity to both methacholine and pentagastrin compared with the normal subjects. In both patients who underwent an overnight manometric study, the LES exhibited cyclic phasic contractile activity synchronous with gastric contractions during the migrating motor complex. We conclude that the study findings support the hypothesis that postganglionic cholinergic LES innervation in achalasia patients is either normal or only minimally impaired, in contrast to the marked impairment of the inhibitory nerves governing LES relaxation.
人们认为，人类食管下括约肌（LES）由非肾上腺素能、非胆碱能抑制神经以及胆碱能兴奋神经支配。在特发性贲门失弛缓症中，LES松弛异常，因为支配该括约肌的抑制神经要么缺失，要么功能受损。然而，支配LES的胆碱能兴奋神经的完整性尚未得到充分评估。我们以27例未经治疗的特发性贲门失弛缓症患者和21名健康志愿者为研究对象，探讨贲门失弛缓症患者中支配LES的节后胆碱能神经功能是否完整这一假设。评估了LES对阿托品、依酚氯铵、乙酰甲胆碱、亚硝酸异戊酯和五肽胃泌素的反应。对2例贲门失弛缓症患者，在夜间测压研究期间观察LES的空腹运动活动模式。贲门失弛缓症患者的LES静息压显著高于正常受试者，分别为41±4 mmHg（平均值±标准误）和20±2 mmHg。阿托品使两组的LES压力均显著降低30%-75%。依酚氯铵使贲门失弛缓症患者的LES压力升高，但对正常受试者影响可忽略不计。与正常受试者相比，贲门失弛缓症患者的LES对乙酰甲胆碱和五肽胃泌素的敏感性均增加。在接受夜间测压研究的2例患者中，LES在移行性运动复合波期间均表现出与胃收缩同步的周期性阶段性收缩活动。我们得出结论，研究结果支持以下假设：与支配LES松弛的抑制神经明显受损相反，贲门失弛缓症患者的节后胆碱能LES神经支配要么正常，要么仅轻微受损。
