Feldman M, Blair A J, Richardson C T
J Clin Invest. 1987 Jun;79(6):1615-20. doi: 10.1172/JCI112997.
We calculated gastric HCO3- and H+ secretion, as well as nonparietal and parietal volume secretion, in 15 duodenal ulcer patients who had previously undergone successful proximal gastric vagotomy, 15 unoperated duodenal ulcer patients, and 15 normal control subjects. Basal HCO3- secretion was not significantly altered after vagotomy, while basal H+ secretion, parietal volume and nonparietal volume secretion were reduced significantly. Intravenous gastrin-17 infusion reduced gastric HCO3- secretion by approximately 50% in both unoperated ulcer patients and normal subjects (P less than 0.05). Gastrin-17 infusion did not inhibit gastric HCO3- secretion after vagotomy. In fact, mean gastric HCO3- secretion increased to a nearly significant extent in response to gastrin (P = 0.06). These findings indicate that gastrin inhibits gastric HCO3- secretion in humans and that the gastrin-induced reduction in gastric HCO3- secretion is dependent upon intact vagal innervation to the oxyntic mucosa.
我们计算了15例先前接受过成功近端胃迷走神经切断术的十二指肠溃疡患者、15例未接受手术的十二指肠溃疡患者以及15例正常对照者的胃HCO₃⁻和H⁺分泌,以及非壁细胞和壁细胞容量分泌。迷走神经切断术后基础HCO₃⁻分泌无显著改变,而基础H⁺分泌、壁细胞容量和非壁细胞容量分泌显著降低。静脉输注胃泌素-17使未接受手术的溃疡患者和正常受试者的胃HCO₃⁻分泌减少约50%(P<0.05)。迷走神经切断术后,胃泌素-17输注未抑制胃HCO₃⁻分泌。事实上,胃泌素刺激后,胃HCO₃⁻平均分泌增加至接近显著水平(P = 0.06)。这些发现表明,胃泌素抑制人类胃HCO₃⁻分泌,且胃泌素诱导的胃HCO₃⁻分泌减少依赖于胃黏膜壁细胞完整的迷走神经支配。