Wolfe M M, Hocking M P, Maico D G, McGuigan J E
Gastroenterology. 1983 May;84(5 Pt 1):941-8.
Previous studies have questioned the physiological role of gastric inhibitory peptide in inhibiting gastric acid secretion. The present study was designed to examine and compare peptone meal-stimulated gastric acid secretion in dogs after intravenous infusion of rabbit serum containing antibodies to gastric inhibitory peptide or normal rabbit serum (as control). Five dogs were prepared with gastric fistulas. Basal acid output was collected for 90 min through the gastric fistula. After 30 min of basal acid output collection, either rabbit serum containing antibodies to gastric inhibitory peptide or normal control rabbit serum (0.1 ml/kg) was infused intravenously over 1 min. After the basal acid output collection, a 10% peptone meal was infused into the stomach. Gastric acid output was measured by intragastric titration (pH 5.0) for 60 min. Peripheral venous plasma was collected for measurement of gastrin and gastric inhibitory peptide and for binding of endogenous plasma gastric inhibitory peptide by administered antibodies to gastric inhibitory peptide before and at 2, 5, 10, 15, 30, 60, 90, and 120 min after the meal. After intravenous administration of antibodies to gastric inhibitory peptide, 98% +/- 3% (SEM) of endogenous plasma gastric inhibitory peptide was bound by administered antibodies to gastric inhibitory peptide. No binding of endogenous plasma gastric inhibitory peptide was detected after infusion of normal rabbit serum. In dogs receiving intravenous antibodies to gastric inhibitory peptide, both peptone-stimulated gastric acid output and integrated gastrin release responses were increased when compared with dogs receiving normal rabbit serum. With infusion of antibodies to gastric inhibitory peptide, there was a high degree of correlation between the increase in gastric acid output and the increase in integrated gastrin response (r = 0.900, p less than 0.04) that followed the peptone meal. This study, using antibodies to bind endogenous gastric inhibitory peptide, demonstrates the capacity of circulating gastric inhibitory peptide to inhibit meal-stimulated gastric acid secretion. Furthermore, these results support the conclusion that this enterogastrone effect of gastric inhibitory peptide is due, at least in part, to inhibition of gastrin release.
以往的研究对胃抑制肽在抑制胃酸分泌中的生理作用提出了质疑。本研究旨在检测和比较静脉输注含抗胃抑制肽抗体的兔血清或正常兔血清（作为对照）后，蛋白胨餐刺激犬胃酸分泌的情况。选用5只犬制作胃瘘。通过胃瘘收集90分钟的基础胃酸分泌量。在收集基础胃酸分泌量30分钟后，将含抗胃抑制肽抗体的兔血清或正常对照兔血清（0.1 ml/kg）在1分钟内静脉输注。收集基础胃酸分泌量后，将10%的蛋白胨餐注入胃内。通过胃内滴定法（pH 5.0）测量60分钟的胃酸分泌量。在进食前以及进食后2、5、10、15、30、60、90和120分钟采集外周静脉血浆，用于测量胃泌素和胃抑制肽，并用于检测注入的抗胃抑制肽抗体对内源性血浆胃抑制肽的结合情况。静脉注射抗胃抑制肽抗体后，98%±3%（标准误）的内源性血浆胃抑制肽被注入的抗胃抑制肽抗体结合。输注正常兔血清后，未检测到内源性血浆胃抑制肽的结合。与接受正常兔血清的犬相比，接受静脉注射抗胃抑制肽抗体的犬，蛋白胨刺激的胃酸分泌量和胃泌素释放综合反应均增加。随着抗胃抑制肽抗体的输注，胃酸分泌量的增加与蛋白胨餐后胃泌素综合反应的增加之间存在高度相关性（r = 0.900，p < 0.04）。本研究使用抗体结合内源性胃抑制肽，证明了循环中的胃抑制肽具有抑制餐食刺激胃酸分泌的能力。此外，这些结果支持以下结论：胃抑制肽的这种肠抑胃素作用至少部分归因于对胃泌素释放的抑制。
