Mogard M, Böttcher W, Kauffman G L, Washington J, Walsh J H
Scand J Gastroenterol. 1986 Jan;21(1):97-103. doi: 10.3109/00365528609034630.
The present study in the dog evaluates neurotensin as a potential hormone, mediating the inhibition of gastric acid secretion by duodenal acidification. Histamine-stimulated acid output was determined before and during duodenal acidification. Portal vein blood was obtained and assayed for carboxy-terminal neurotensin-like immunoreactivity (NTLI). Duodenal perfusion with 15 mmol HCL for 30 min significantly inhibited histamine-stimulated acid output to 67% of control output. This inhibition was not associated with any change in the peripheral plasma NTLI, but the portal plasma NTLI was significantly elevated from 27 to 78 pM. The effect of duodenal acidification on liver extract meal-stimulated acid secretion was determined in a second group of dogs without portal vein catheter. Duodenal perfusion with 15 mmol HCl for 30 min significantly inhibited meal-stimulated acid secretion to 37% of control output. Intravenous infusion of synthetic neurotensin to a plasma level of 130 pM was required to inhibit meal-stimulated acid output significantly. In summary, NTLI is elevated in portal, but not peripheral, plasma after duodenal acidification. The associated inhibition of acid secretion is not due to hormonal action of neurotensin.
本项针对犬类的研究评估了神经降压素作为一种潜在激素，介导十二指肠酸化对胃酸分泌的抑制作用。在十二指肠酸化之前和期间测定组胺刺激的酸分泌量。采集门静脉血并检测其羧基末端神经降压素样免疫反应性（NTLI）。用15 mmol盐酸对十二指肠进行30分钟灌注，可显著抑制组胺刺激的酸分泌量至对照分泌量的67%。这种抑制作用与外周血浆NTLI的任何变化均无关，但门静脉血浆NTLI从27 pM显著升高至78 pM。在第二组未插入门静脉导管的犬类中，测定十二指肠酸化对肝提取物餐刺激的酸分泌的影响。用15 mmol盐酸对十二指肠进行30分钟灌注，可显著抑制餐刺激的酸分泌至对照分泌量的37%。需要静脉输注合成神经降压素使血浆水平达到130 pM才能显著抑制餐刺激的酸分泌量。总之，十二指肠酸化后门静脉血浆而非外周血浆中的NTLI升高。酸分泌的相关抑制并非由于神经降压素的激素作用。
