Gastric acid secretion is abnormally sensitive to endogenous gastrin released after peptone test meals in duodenal ulcer patients.
Gastric acid secretion is abnormally sensitive to endogenous gastrin released after peptone test meals in duodenal ulcer patients.
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十二指肠溃疡患者的胃酸分泌对蛋白胨测试餐后释放的内源性胃泌素异常敏感。
DOI：
10.1172/jci109699
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
J. Walsh
中科院分区：
文献类型：
--
作者：
S. Lam;J. Isenberg;M. Grossman;W. H. Lane;J. Walsh
我们研究了25名十二指肠溃疡患者和14名年龄和性别匹配的正常对照组，以确定十二指肠溃疡患者的胃酸分泌是否对内源性胃泌素的刺激异常敏感。用30min胃内滴定的方法测定小鼠对生理盐水和0.5、1.0、2.0、4.0、8.0%蛋白胨灌胃的胃酸反应。用放射免疫法测定空腹和餐后30min的血清总胃泌素(G-TOTAL)和血清七肽胃泌素(G17)。在19例溃疡患者和11例正常人(对照组)中，还测定了G17-I对分级剂量(11、33、100和300pmol kg(-1)h(-1))的酸反应。十二指肠球部溃疡患者对每一剂量蛋白酵素的平均产酸量显著高于对照组。溃疡患者和对照组的胃泌素水平无显著差异。在个体患者和对照组中，G-TOTAL和G17与餐激酸排出量显著相关，无论是检查绝对酸排量、基础校正酸排量还是膨胀校正酸排量(中位数r范围为0.82至0.94P<；0.001)。从各个回归线中，计算出与观察到的最高餐激酸反应(D(50M))的一半相对应的胃泌素浓度。十二指肠溃疡患者的G-TOTAL和G17的平均D(50M)显著低于对照组，无论是在总体组中，还是在两组溃疡患者和对照组中，根据观察到的最高膳食刺激酸反应或根据合成的人G17反应的最大酸量进行匹配。外源性给予G17所需的剂量为G17酸反应平均值D的一半(50g)，患者组显著低于对照组。在溃疡和对照组中，D(50g)与D(50m)显著相关。这一点以及膳食刺激的G17和胃酸反应之间的显著相关性强烈地表明，内源性释放的胃泌素负责大部分(如果不是全部)蛋白妥钠后酸的输出。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的刺激异常敏感。
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.