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一种用于抗酸剂体外评估的人工胃十二指肠模型。

An artificial stomach-duodenum model for the in-vitro evaluation of antacids.

作者信息

Vatier J, Malikova-Sekera E, Vitre M T, Mignon M

机构信息

INSERM Unit 10, Hôpital Xavier Bichat, Paris, France.

出版信息

Aliment Pharmacol Ther. 1992 Aug;6(4):447-58. doi: 10.1111/j.1365-2036.1992.tb00558.x.

Abstract

To improve the dynamic in-vitro evaluation of the effects of antacids, we have developed the 'artificial stomach' model by adding a 'duodenal reservoir' to receive the gastric emptying flux and simulated bicarbonate secretion, thus constituting an 'artificial stomach-duodenum' model. With this model we measured antacid-induced resistance to gastric acidification, and simultaneously evaluated the effect of antacid activity on the duodenal milieu. The model also permitted evaluation of the antacid effects of proteins (as natural antacids), and of drugs containing aluminium phosphate, alone or combined with magnesium oxide, or aluminium and magnesium hydroxides. At the gastric site, these drugs, as well as the proteins (that is, meat extract), induced a strong resistance to acidification due to the gastric emptying flux and to antacid composition. At the duodenal site, the decrease of the acid load penetrating into the duodenum varied, depending on the efficacy of gastric antacid activity. Duodenal pH was related to the equilibrium between bicarbonate secretion and the emptying of acid load. Proteins and aluminium phosphate induced the same duodenal pH as in the control tests without antacids, but magnesium-containing antacids increased it, thus decreasing bicarbonate consumption. The antacid mechanisms within the stomach, and the fate of antacids in the duodenal milieu, might explain the variation in duodenal pH in response to antacid administration.

摘要

为了改进抗酸剂作用的动态体外评估,我们通过添加一个“十二指肠储器”来接收胃排空流量并模拟碳酸氢盐分泌,从而开发了“人工胃”模型,进而构建了一个“人工胃 - 十二指肠”模型。利用该模型,我们测量了抗酸剂诱导的对胃酸化的抵抗作用,并同时评估了抗酸活性对十二指肠环境的影响。该模型还允许评估蛋白质(作为天然抗酸剂)以及含磷酸铝的药物单独或与氧化镁或氢氧化铝和氢氧化镁组合使用时的抗酸效果。在胃部,这些药物以及蛋白质(即肉提取物)由于胃排空流量和抗酸剂成分而对酸化产生强烈的抵抗作用。在十二指肠部位,渗透到十二指肠的酸负荷的降低程度各不相同,这取决于胃抗酸活性的功效。十二指肠pH值与碳酸氢盐分泌和酸负荷排空之间的平衡有关。蛋白质和磷酸铝诱导的十二指肠pH值与无抗酸剂的对照试验中的相同,但含镁抗酸剂会使其升高,从而减少碳酸氢盐的消耗。胃内的抗酸机制以及抗酸剂在十二指肠环境中的去向,可能解释了十二指肠pH值因施用抗酸剂而产生变化的原因。

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