Holstein B, Cederberg C
Acta Physiol Scand. 1980 May;109(1):37-44. doi: 10.1111/j.1748-1716.1980.tb06561.x.
Cods were prepared for measurement of gastric acid secretion. Cannulae were implanted for drainage of the stomach and for separate perfusion of the stomach and intestine. Fishes, intestinally perfused with diluted sea-water (33% SW) exhibited high rates of acid secretion. This "basal" secretion was abolished (96% inhibition) by bilateral vagotomy. Perfusion of the stomach with isosmotic glucose (5.5%) diminished the amount of titratable acid in the gastric effluence, and induced oral ingestion of water. Only part of the decrease could be explained by neutralization by ingested sea-water. Perfusion of the intestine with 5.5% glucose, containing sea-water to raise the osmolality to that of 50% SW, depressed gastric acid secretion compared to 50% SW-perfused controls, without significantly affecting oral intake of water. I.m. administration of glucose, increasing plasma glucose to the same level as intraluminal administration, did not affect acid secretion or oral water ingestion. The study demonstrates the existence of a potential intestinal mechanism for inhibition of gastric acid secretion, and indicates that vagal activity is independent of the blood glucose level in the cod.
将鳕鱼制备用于测量胃酸分泌。植入套管用于胃引流以及胃和肠的单独灌注。用稀释海水（33%海水）进行肠灌注的鱼类表现出高胃酸分泌率。这种“基础”分泌通过双侧迷走神经切断术被消除（96%抑制）。用等渗葡萄糖（5.5%）灌注胃减少了胃流出物中可滴定酸的量，并引发了经口饮水。减少的部分中只有一部分可以用摄入的海水中和来解释。用含有海水以将渗透压提高到50%海水渗透压的5.5%葡萄糖灌注肠，与用50%海水灌注的对照组相比，胃酸分泌受到抑制，但对经口摄水量没有显著影响。肌肉注射葡萄糖使血浆葡萄糖升高到与腔内给药相同水平，对胃酸分泌或经口饮水没有影响。该研究证明存在一种潜在的肠道抑制胃酸分泌机制，并表明迷走神经活动在鳕鱼中与血糖水平无关。
