Vatier J, Poitevin C, Vitré M T, Mignon M
INSERM U-10, Unité de Recherche de Gastroentérologie, CHU Xavier-Bichat, Paris.
Gastroenterol Clin Biol. 1988 Mar;12(3):207-13.
The high choline content in pancreatic juice and bile-contaminated gastric juice samples suggested that intragastric choline content could be related to duodenogastric reflux (DGR). In 308 secretory tests in normal subjects (38) and in duodenal ulcer patients (DU) (270), acid, pepsin, sialic acid and choline outputs were measured in basal secretion and after pentagastrin, insulin or secretin modulation. The distribution of choline output values in basal secretion showed that 77% subjects had no or small choline amounts (less than 10 mumol/h) and another population had high output values (greater than or equal to 10 mumol/h). Choline hourly outputs greater than or equal to 10 mumol/h could be related with positive DGR. DGR did not seem to modify acid or pepsin secretion except if acid outputs were low: in these cases the neutralizing activity reduced acid outputs and resulted in a pepsin inactivation. DGR by itself increased sialic acid outputs as evidenced by mucus erosion. In normal subjects, weak mucus erosion might be due to proteolytic activity. In DU patients without DGR, erosion was increased but was due to the same mechanism. In DU patients with DGR, erosion was stronger and no relationship with proteolytic activity could be established because of the introduction of eroded duodenal glycoprotein into the stomach. Pentagastrin, insulin and secretin were able to induce DGR. Reflux could contribute to mucus erosion either by its detersive properties or by the proteolytic material coming from the pancreas.
胰液和胆汁污染的胃液样本中胆碱含量较高,这表明胃内胆碱含量可能与十二指肠-胃反流(DGR)有关。在对正常受试者(38例)和十二指肠溃疡患者(DU,270例)进行的308次分泌试验中,测量了基础分泌以及在五肽胃泌素、胰岛素或促胰液素调节后酸、胃蛋白酶、唾液酸和胆碱的分泌量。基础分泌中胆碱分泌量值的分布表明,77%的受试者胆碱含量无或很少(低于10 μmol/h),另一部分受试者胆碱分泌量值较高(大于或等于10 μmol/h)。胆碱每小时分泌量大于或等于10 μmol/h可能与阳性DGR有关。除了酸分泌量较低的情况外,DGR似乎不会改变酸或胃蛋白酶的分泌:在这些情况下,中和活性会降低酸分泌量并导致胃蛋白酶失活。如黏液糜烂所示,DGR本身会增加唾液酸分泌量。在正常受试者中,轻微的黏液糜烂可能是由于蛋白水解活性。在无DGR的DU患者中,糜烂增加但机制相同。在有DGR的DU患者中,糜烂更严重,且由于十二指肠糖蛋白侵蚀物进入胃内,无法确定其与蛋白水解活性的关系。五肽胃泌素、胰岛素和促胰液素能够诱导DGR。反流可能因其去污特性或来自胰腺的蛋白水解物质而导致黏液糜烂。