Lam S K, Isenberg J I, Grossman M I, Lane W H, Walsh J H
J Clin Invest. 1980 Feb;65(2):555-62. doi: 10.1172/JCI109699.
We studied 25 duodenal ulcer patients and 14 age- and sex-matched normal controls to determine whether gastric acid secretion in duodenal ulcer patients is abnormally sensitive to stimulation by gastrin endogenously released in response to meals. Acid response to saline and to 0.5, 1.0, 2.0, 4.0, and 8.0% peptone infused into the stomach was measured by 30 min intragastric titration. Total serum gastrin (G-total) and serum heptadecapeptide gastrin (G17), fasting and 30 min after each test meal, were measured by specific radioimmunoassays. In 19 ulcer patients and 11 normal subjects (controls), acid response to graded doses (11, 33, 100, and 300 pmol kg(-1) h(-1)) of G17-I were also measured. Mean acid output in response to each dose of peptone was significantly higher in duodenal ulcer patients than in the controls. Gastrin levels in ulcer patients and controls were not significantly different. Within individual patients and controls, both G-total and G17 were significantly correlated with meal-stimulated acid output regardless of whether the absolute, basal-corrected, or distention-corrected values for acid output were examined (median r ranged from 0.82 to 0.94, P < 0.001). From the individual regression lines, the gastrin concentrations corresponding to half of the highest observed meal-stimulated acid response (D(50m)) were calculated. Mean D(50m) for G-total and G17 were significantly lower in duodenal ulcer patients than in controls both in the overall group and in pairs of ulcer patients and controls matched on the basis of highest observed meal-stimulated acid responses, or on the basis of maximal acid output in response to synthetic human G17. The dose of exogenously administered G17 required for half maximal G17 acid response mean D(50g), was significantly less in patients than in control subjects. In both ulcer and control subjects, D(50g) correlated significantly with D(50m). This and the significant correlation between meal-stimulated G17 and acid response strongly suggest that the endogenously released gastrin was responsible for most, if not all, of the postpeptone acid output.We conclude that after peptone test meals, gastric acid secretion in duodenal ulcer patients was abnormally sensitive to stimulation by endogenously released gastrin.
我们研究了25例十二指肠溃疡患者和14例年龄及性别匹配的正常对照者，以确定十二指肠溃疡患者的胃酸分泌对因进食而内源性释放的胃泌素刺激是否异常敏感。通过30分钟胃内滴定法测量对注入胃内的生理盐水以及0.5%、1.0%、2.0%、4.0%和8.0%蛋白胨的酸反应。通过特异性放射免疫测定法测量每次试验餐后空腹及餐后30分钟时的血清总胃泌素（G-总）和血清十七肽胃泌素（G17）。在19例溃疡患者和11例正常受试者（对照）中，还测量了对不同剂量（11、33、100和300 pmol kg⁻¹ h⁻¹）G17-I的酸反应。十二指肠溃疡患者对各剂量蛋白胨的平均酸排出量显著高于对照组。溃疡患者和对照组的胃泌素水平无显著差异。在个体患者和对照中，无论检查酸排出量的绝对值、基础校正值还是扩张校正值，G-总和G17均与进餐刺激的酸排出量显著相关（中位数r范围为0.82至0.94，P<0.001）。根据个体回归线，计算出与最高观察到的进餐刺激酸反应的一半相对应的胃泌素浓度（D(50m)）。在总体组以及根据最高观察到的进餐刺激酸反应或根据对合成人G17的最大酸排出量匹配的溃疡患者和对照对中，十二指肠溃疡患者的G-总和G17的平均D(50m)均显著低于对照组。达到最大G17酸反应一半所需的外源性给予G17的剂量（平均D(50g)），患者显著低于对照受试者。在溃疡和对照受试者中，D(50g)与D(50m)均显著相关。这一点以及进餐刺激的G17与酸反应之间的显著相关性强烈表明，内源性释放的胃泌素至少对大部分（如果不是全部）蛋白胨后酸排出量负责。我们得出结论，在蛋白胨试验餐后，十二指肠溃疡患者的胃酸分泌对内源性释放的胃泌素刺激异常敏感。
