Gastroduodenal reflux material effect (1) gastric acid and pepsin on the esophageal injury. Matter of acid reflux on esophageal mucosa and protease injury. On gastric acid and pepsin on the esophageal mucosa in GERD damage in the role of literature arguing less. Early animal experiments show that different concentrations of acid and pepsin damage effect on the esophageal mucosa. Jodson other single infusion of rabbit esophagus with hydrochloric acid and found that less mucosal injury, but with different concentrations of pepsin and hydrochloric acid infusion at the same time, the injury serious. Application of pH monitoring confirmed that 90% of reflux esophagitis and Barrett esophagus patients whose esophageal acid exposure time on. Bremner and other esophageal pH monitor with a 24h monitoring of GERD and controls, monitoring data show that the biggest trends in esophageal mucosal injury mainly in pH0_2 and pH7_8 between. In vivo experiments confirmed that pH0_2 level, the maximum activity of pepsin may be due to acid activation of pepsin caused the damage to the esophageal mucosa, and not directly the result of acid. Blaclkshaw by ship rats and other studies have found that esophageal acid can lead to peripheral afferent nerve terminals in the release of substance P, P substance through the activation of Neurokinin-1 receptor, leading to LES relaxation.
In addition, 10% _15%, although the typical symptoms of patients, but endoscopic examination was normal, 24hpH monitoring are normal, that is, without acid reflux. There are two assumptions about its causes: the existence of these patients reflux, but reflux is neutral. Under these conditions, bile salts, etc. produced on non-specific esophageal mucosal injury. These patients had abnormal esophageal motility, or called "irritation esophagus." Eriksen and other mass with a radionuclide esophageal transit of solid marker technology confirmed that 50% of patients had abnormal esophageal peristalsis, 2 / 3 of patients present in the second half segment of esophageal peristalsis.
Gastroduodenal reflux material effect (2) duodenal juice on the esophageal injury. Bile acids in the mechanism of action in GERD is not very clear. Early animal experiments confirmed that bile acid induced esophageal mucosal damage depends on the combination of bile acid reflux liquid state and pH. Combination of acid and non-binding Glycocholic acid pH greater than 4, the pH <4 when precipitated, while the combination of taurocholic acid at pH 2 when dissolved. Esophageal acid through the net amount (NAF) as the damage index, Harmon of membrane damage in rabbit esophagus Ru found: with taurocholic acid (taurocholic acid and oxygen taurocholic acid) at pH of 2 NAF increased with the state rather than in pH 7 NAF increased. Under acidic conditions, combined with acid on large esophageal mucosal damage; not when combined with acid in pH5_8 damaging large. Research on the human body by esophageal suction technology, the aspirates were analyzed. Nehra, etc. found that bile flow is a variable anti-pH range, while the majority of bile reflux with acid reflux, known as the mixed reflux (acid and bile). Esophageal reflux is such a serious injury, the main form. Reflux material in the main components of the primary bile acid, that is, taurocholic acid, ammonia acid and bile Gan. Taurocholic acid in Barrett esophagus stenosis was significantly increased, and the concentration of taurocholic acid in combination with acid-related and strong. Under acidic conditions, combined with taurocholic acid is an important factor in causing mucosal injury. Therefore, compounds that pH reflux by affecting the concentration of bile acids, thus affecting its toxicity. Acid and bile in the pathogenesis of a synergistic effect. Also contained in bile, duodenal juice, the membrane enzyme can also cause esophageal mucosal damage, combined with acid only in the acidic environment of mucosal injury, and not with acid in an alkaline environment and with the destruction of esophageal mucosal membrane enzymes.
Gastroduodenal reflux material effect, the membrane protein's role in GERD controversial, Kivilaakso rabbit esophagus in vitro study found that when the pH is 3.5, taurocholic acid pot, lysophosphatidylcholine, pepsin on produce mucosal damage; at pH 7.4, the non-binding bile acids, membrane protein, phospholipase A production of mucosal damage. Gatley, etc. found in GERD patients with reflux material in the membrane protein concentration is very low, that in the acidic environment of the stomach to reach through the esophagus, the membrane protein structure vulnerable to complete destruction of much of esophageal mucosal injury.