Abstract
It was proposed by Pavlov already in 1898 [26] that “alkaline mucus” lining the gastric mucosa neutralized luminal acid and that it had a protective role. Many years later, Hollander postulated the occurrence of gastric secretion of an alkaline (non-parietal fluid) and that this fluid was produced at a constant rate [15]. He also demonstrated the occurrence of bicarbonate in the secretion from gastric fundic pouches in dogs after inhibition of the acid secretion by vagotomy and antrectomy. During the last ten years it has been found in all species tested that gastric antral and fundic mucosa secretes bicarbonate to the lumen and that this secretion can be stimulated and inhibited by a variety of means. The secretion most probably originates from the surface epithelial cells. Furthermore, the surface epithelium in duodenal segments devoid of Brunner’s glands possesses a similarly metabolism dependent secretion of bicarbonate. The rates of secretion (per unit surface area) are higher in the duodenum than in the stomach and higher in proximal than in more distal segments of the duodenum. In addition, there are distinct differences between the duodenum and the stomach with respect to both the processes of transport of bicarbonate and pathways for stimulation of the secretion [8, 9].
This work was supported by the Swedish Medical Research Council: grant 04X-3515.
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Flemström, G. (1988). Gastroduodenal Bicarbonate Secretion in Mucosal Protection. In: Domschke, W., Dammann, H.G., Peskar, B.M., Holtermüller, K.H. (eds) Prostaglandins and Leukotrienes in Gastrointestinal Diseases. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73316-1_22
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