Lloyd K C, Hölzer H H, Zittel T T, Raybould H E
Research Service, Department of Veterans Affairs, West Los Angeles Medical Center, California.
Am J Physiol. 1993 Apr;264(4 Pt 1):G659-63. doi: 10.1152/ajpgi.1993.264.4.G659.
Neural and endocrine pathways mediate the inhibitory effects of intestinal fat on gastric acid secretion. To study whether vagal and/or spinal afferent nerves contribute to the neural component of the enterogastric reflex, the sensory neurotoxin capsaicin was applied topically either to the vagus nerves bilaterally or to the celiac-superior mesenteric ganglia in rats with chronic gastric and duodenal fistulas. In lightly restrained, awake rats acid secretion was stimulated for 2 h by continuous intragastric perfusion with 8% peptone and was measured by extragastric titration to pH 5.5. Duodenal lipid perfusion (0-20%) during the 2nd h caused inhibition of peptone-stimulated acid output. Acid output was inhibited by 81% during 5% lipid perfusion of the duodenum and was restored after capsaicin treatment of the vagus nerves. In contrast, capsaicin treatment of the celiac ganglion did not alter the acid inhibitory response to any dose of intestinal lipid. Basal and maximum acid outputs were not significantly different among rats treated by either method with capsaicin. The neural component of the enterogastric reflex in awake rats is mediated in part by a capsaicin-sensitive, vagal-afferent neural reflex.
神经和内分泌途径介导肠道脂肪对胃酸分泌的抑制作用。为了研究迷走神经和/或脊髓传入神经是否参与肠胃反射的神经成分，将感觉神经毒素辣椒素局部应用于双侧迷走神经或患有慢性胃和十二指肠瘘的大鼠的腹腔 - 肠系膜上神经节。在轻度约束的清醒大鼠中，通过用8%蛋白胨连续胃内灌注刺激胃酸分泌2小时，并通过胃外滴定至pH 5.5来测量。在第2小时十二指肠脂质灌注（0 - 20%）导致蛋白胨刺激的酸分泌受到抑制。在十二指肠5%脂质灌注期间，酸分泌受到81%的抑制，在对迷走神经进行辣椒素处理后恢复。相比之下，对腹腔神经节进行辣椒素处理并没有改变对任何剂量肠道脂质的酸抑制反应。用两种方法之一用辣椒素处理的大鼠之间的基础酸分泌和最大酸分泌没有显著差异。清醒大鼠肠胃反射的神经成分部分由辣椒素敏感的迷走神经传入神经反射介导。
