Orloff S L, Bunnett N W, Walsh J H, Debas H T
Department of Physiology, University of California, San Francisco 94143.
Am J Physiol. 1992 Jan;262(1 Pt 1):G165-70. doi: 10.1152/ajpgi.1992.262.1.G165.
To determine the relative contributions of neural reflexes and intestinal hormones to the inhibition of gastric acid secretion by intestinal acidification, rats with an extrinsically denervated, transplanted segment of jejunum, and those with an innervated segment of jejunum, were studied. Postoperatively, meal-stimulated gastric acid secretion was measured. When the acid secretory response to intragastric liver extract reached a plateau, graded concentrations of hydrochloric acid or saline were instilled into the jejunal segments. Gastric acid secretion was inhibited by intrajejunal acid (pH 2.5) by 79% in the innervated rats and by 64% in the transplanted group. Thus at a pH of 2.5 there was a 15% greater maximum inhibition of plateau acid response in the innervated rats than in the transplanted rats, presumably because of the extrinsic neural contribution. To examine the hormonal mediators, the effects of a somatostatin monoclonal antibody and a CCK-A receptor antagonist (L 364718) on acid-induced inhibition of gastric acid secretion were studied in transplanted rats. Treatment with a somatostatin monoclonal antibody or with L 364718 reduced the acid-induced (pH 2.5) inhibition of gastric acid secretion by 93 and 27%, respectively. Jejunal acidification inhibits gastric acid secretion in the rat by both neural and hormonal mechanisms. The hormonal mechanism is mediated by somatostatin and CCK.
为了确定神经反射和肠激素在肠酸化抑制胃酸分泌过程中的相对作用,研究了具有外在去神经支配的空肠移植段的大鼠以及具有空肠神经支配段的大鼠。术后,测量进食刺激后的胃酸分泌。当对胃内肝提取物的酸分泌反应达到平台期时,将不同浓度的盐酸或生理盐水注入空肠段。空肠内酸(pH 2.5)使有神经支配的大鼠胃酸分泌抑制79%,移植组抑制64%。因此,在pH 2.5时,有神经支配的大鼠比移植大鼠的平台期酸反应最大抑制率高15%,这可能是由于外在神经的作用。为了研究激素介质,在移植大鼠中研究了生长抑素单克隆抗体和CCK - A受体拮抗剂(L 364718)对酸诱导的胃酸分泌抑制的影响。用生长抑素单克隆抗体或L 364718处理分别使酸诱导的(pH 2.5)胃酸分泌抑制降低了93%和27%。空肠酸化通过神经和激素机制抑制大鼠胃酸分泌。激素机制由生长抑素和CCK介导。