Yamagishi T, Debas H T
Ann Surg. 1981 Mar;193(3):324-30. doi: 10.1097/00000658-198103000-00012.
This study examines the effect of graded antral distension with acid (0.1 M HCl) or alkali (0.1 M NaHCO3) on pentagastrin-stimulated acid secretion in two groups of dogs. Group A consisted of six dogs provided with innervated antral pouch. In these dogs, the vagal branches to the fundus, as well as the extragastric vagal divisions (hepatic and celiac), were preserved. All of these animals had a gastric fistula in the main stomach, and in two a denervated fundic pouch or Heidenhain pouch was constructed in addition. Group B consisted of four dogs with an innervated antral pouch and gastric fistula. In this latter group, however, parietal cell vagotomy as well as extragastric vagotomy (division of the hepatic and celiac branches) was performed so that the only vagal communication was between the antrum and the CNS. Antral distension with acid caused significant inhibition of pentagastrin-stimulated acid secretion from both the gastric fistula and the Heidenhain pouch in Group A dogs. Antral acidification without distension did not inhibit. Alkaline antral distension in this group caused much less inhibition of acid secretion, but did cause significant increase in circulating immunoreactive gastrin. In Group B dogs, antral distension with neither acid nor alkali caused inhibition of pentagastrin-stimulated acid secretion, indicating that intact vagal supply to the oxyntic mucosa and/or to the extragastric abdominal organs is necessary for the inhibitory mechanism to operate. The results of this study suggest that: a) antral acidification per se does not inhibit pentagastrin-stimulated acid secretion; and b) antral distension with acid, and to a lesser extent with alkali, is inhibitory only if vagal innervation to the fundus and other abdominal viscera is preserved. The observations are compatible with the hypothesis that antral distension activates a neurohumoral inhibitory mechanism releasing the inhibitor reflexly from sites other than the antrum or CNS.
本研究检测了用酸（0.1M盐酸）或碱（0.1M碳酸氢钠）对两组犬进行分级胃窦扩张，对五肽胃泌素刺激的胃酸分泌的影响。A组由6只具备有神经支配的胃窦小袋的犬组成。在这些犬中，保留了至胃底的迷走神经分支以及胃外迷走神经分支（肝支和腹腔支）。所有这些动物的主胃均有胃瘘，其中2只还另外构建了去神经支配的胃底小袋或海登海因小袋。B组由4只有神经支配的胃窦小袋和胃瘘的犬组成。然而，在这后一组中，进行了壁细胞迷走神经切断术以及胃外迷走神经切断术（肝支和腹腔支切断），使得唯一的迷走神经联系存在于胃窦和中枢神经系统之间。用酸进行胃窦扩张导致A组犬胃瘘和海登海因小袋中五肽胃泌素刺激的胃酸分泌受到显著抑制。无扩张的胃窦酸化则无抑制作用。该组中用碱进行胃窦扩张对胃酸分泌的抑制作用小得多，但确实导致循环中免疫反应性胃泌素显著增加。在B组犬中，用酸或碱进行胃窦扩张均未抑制五肽胃泌素刺激的胃酸分泌，这表明胃酸分泌抑制机制发挥作用需要对泌酸黏膜和/或胃外腹部器官有完整的迷走神经支配。本研究结果提示：a）胃窦酸化本身并不抑制五肽胃泌素刺激的胃酸分泌；b）仅当至胃底和其他腹部脏器的迷走神经支配保留时，用酸进行胃窦扩张以及程度较轻的用碱进行胃窦扩张才具有抑制作用。这些观察结果与如下假说相符，即胃窦扩张激活了一种神经体液抑制机制，该机制从胃窦或中枢神经系统以外的部位反射性释放抑制剂。
