Lenz H J, Hogan D L, Isenberg J I
Gastroenterology. 1985 Oct;89(4):791-6. doi: 10.1016/0016-5085(85)90574-8.
To examine the effect of proximal small intestinal stimulants of gastric acid secretion in cirrhotic patients with portacaval shunt, unshunted cirrhotics, and normal subjects, a mixture of L-amino acids was administered intraduodenally, into the proximal jejunum, or intravenously to 8 cirrhotic patients with portacaval shunt and to 8 unshunted subjects (4 cirrhotic and 4 healthy volunteers). In addition, the effect of intrajejunally administered hyperosmolar mannitol (850 mosmol/kg) and intrajejunal balloon distention (40 mmHg) was determined. In the shunted and unshunted groups gastric acid secretion significantly increased equally in response to intravenous and intraduodenal amino acid infusion, whereas amino acids administered intrajejunally did not significantly alter acid secretion. Perfusion of the jejunum with hyperosmolar mannitol resulted in significant stimulation of acid secretion in the shunted subjects, whereas in the unshunted subjects it caused significant inhibition. In addition, jejunal balloon distention significantly stimulated secretion in the shunted subjects, but not in the unshunted group. Serum gastrin did not change significantly during any of the experiments and plasma amino acids were not different after jejunal compared with duodenal perfusion. These studies indicate the following: Enteral and parenteral amino acids increase gastric acid secretion similarly in subjects with and without portacaval shunt. The intestinal phase of gastric acid secretion is initiated by intraduodenal, but not intrajejunal, amino acids. As plasma amino acid concentrations were similar regardless of the route used, this suggests that the intestinal phase of acid secretion cannot be fully explained by the postabsorptive stimulation by amino acids. Intrajejunal distention with a balloon or infusion of hyperosmolar mannitol into the proximal jejunum stimulates acid secretion only in subjects with portacaval shunt.
为研究近端小肠胃酸分泌刺激物对门腔分流的肝硬化患者、未行分流术的肝硬化患者及正常受试者的影响，将L - 氨基酸混合物经十二指肠内、空肠近端或静脉注射给予8名门腔分流的肝硬化患者及8名未行分流术的受试者（4名肝硬化患者和4名健康志愿者）。此外，还测定了空肠内给予高渗甘露醇（850毫渗摩尔/千克）和空肠内气囊扩张（40毫米汞柱）的效果。在分流组和未分流组中，静脉内和十二指肠内输注氨基酸后胃酸分泌均显著同等增加，而空肠内给予氨基酸并未显著改变胃酸分泌。空肠灌注高渗甘露醇可导致分流受试者的胃酸分泌显著增加，而在未分流受试者中则引起显著抑制。此外，空肠气囊扩张可显著刺激分流受试者的胃酸分泌，但对未分流组无此作用。在任何实验过程中血清胃泌素均无显著变化，空肠灌注后血浆氨基酸与十二指肠灌注后相比无差异。这些研究表明：有或无门腔分流的受试者中，肠内和肠外氨基酸增加胃酸分泌的情况相似。胃酸分泌的肠期由十二指肠内而非空肠内的氨基酸启动。由于无论采用何种途径血浆氨基酸浓度相似，这表明胃酸分泌的肠期不能完全用氨基酸吸收后刺激来解释。空肠内气囊扩张或向空肠近端输注高渗甘露醇仅在门腔分流的受试者中刺激胃酸分泌。
