Galmiche J P, Janssens J
Laboratoire Fonctions Digestives et Nutrition et Clinique de Maladies de l'Appareil Digestif, Université de Nantes, Hôpital, G section R Laënnec, France.
Scand J Gastroenterol Suppl. 1995;211:7-18. doi: 10.3109/00365529509090286.
Gastro-oesophageal reflux disease (GORD) is a multifactorial disease. Although it is primarily a motility disorder, several other disturbances can interfere and contribute to determine the severity of symptoms and the degree of lesions. In normal subjects, as in patients with pathological reflux, nearly all the episodes of reflux obey one of the following three mechanisms: (a) a transient complete relaxation of the lower oesophageal sphincter (TLOSR), (b) a transient increase in intra-abdominal pressure which overcomes the resistance of the antireflux barrier ('stress reflux') and, (c) a spontaneous reflux through a permanently hypotonic sphincter. Gastric distension is the major factor that can induce TLOSRs. Whereas, at rest, the diaphragm probably plays little role in cardial competence, diaphragmatic contraction may help prevent reflux in conditions resulting in increased abdominal pressure such as during physical activity and abdominal staining. The presence of a hiatal hernia increases susceptibility to reflux. A delayed gastric emptying may also facilitate reflux and represents a factor of resistance to antireflux therapy. Most studies in humans have shown that motor abnormalities remain unchanged after healing of oesophagitis. Acid and pepsin are the most noxious agents of the upper gastrointestinal secretions that can participate in the pathogenesis of oesophagitis. However, there is no evidence that patients with reflux have greater acid secretion than subjects without reflux. The clearance function is a two-stage phenomenon requiring first a reduction in volume by peristalsis and then chemical neutralization by saliva. Primary peristalsis is mainly responsible for the clearance of acid in both the upright and the supine positions. It takes longer to clear acid in patients with non-reducing hiatal hernia. The layer of mucus which carpets the mucosa comes from the saliva and also from the submucosal glands of the oesophagus. The paracellular pathway is the major route by which mucosal HCl enters and then damages the oesophageal epithelium. Only a minority of acid reflux episodes are accompanied by symptoms. The acid exposure during the time period that precedes a reflux episode (i.e. the acid burden) is a key factor determining whether that reflux episode will be symptomatic or asymptomatic.
胃食管反流病（GORD）是一种多因素疾病。虽然它主要是一种动力障碍性疾病，但其他一些紊乱也会干扰并促使症状严重程度和病变程度的形成。在正常受试者以及病理性反流患者中，几乎所有反流发作都遵循以下三种机制之一：（a）食管下括约肌一过性完全松弛（TLOSR）；（b）腹内压一过性升高，克服抗反流屏障的阻力（“应激性反流”）；（c）通过永久性低张括约肌的自发性反流。胃扩张是可诱发TLOSR的主要因素。而在静息状态下，膈肌可能对贲门功能影响不大，但在诸如体力活动和腹部用力等导致腹压增加的情况下，膈肌收缩可能有助于防止反流。食管裂孔疝的存在会增加反流易感性。胃排空延迟也可能促进反流，并且是抗反流治疗的一个阻碍因素。大多数人体研究表明，食管炎愈合后运动异常仍无变化。胃酸和胃蛋白酶是上消化道分泌物中最具毒性的物质，可参与食管炎的发病机制。然而，没有证据表明反流患者的胃酸分泌比无反流者更多。清除功能是一个分两个阶段的过程，首先通过蠕动减少容量，然后通过唾液进行化学中和。原发性蠕动主要负责在直立位和仰卧位时清除胃酸。在有不可复位食管裂孔疝的患者中，清除胃酸所需时间更长。覆盖黏膜的黏液层来自唾液以及食管的黏膜下腺。细胞旁途径是黏膜盐酸进入并随后损伤食管上皮的主要途径。只有少数胃酸反流发作伴有症状。反流发作前时间段内的酸暴露（即酸负荷）是决定该反流发作是否有症状的关键因素。
