Gastric glands

The stomach receives food from the buccal cavity, it partially digests protein, fat and carbohydrate and it then delivers the resulting mixture (chyme) into the small intestine. The inner surface of the stomach is folded into ridges, to allow for distension after a meal, they contain gastric pits into which several gastric glands discharge their secretions (Table 4.1). 

The hydrolysis of triacylglycerol is catalysed by lipases, two of which are present in the stomach. These are lingual lipase, which is secreted by the soft palate, and gastric lipase, which is secreted by the gastric glands of the stomach. Gastric lipase is particnlarly important in the newborn since, at this stage of life, pancreatic secretions contain relatively little lipase. 

Histamine also evokes a copious secretion of highly acidic gastric juice from the gastric glands at doses below those that influence blood pressure (32). This effect of histamine is mediated through 2 receptors on the parietal cells. The importance of this effect in scombroid poisoning is not knowi. Histamine also has some stimulant actions on salivary, pancreatic, intestinal, bronchial, and lacrimal secretions (32), but these effects are relatively unimportant. 

Among patients infected with H pylori, long-term acid suppression leads to increased chronic inflammation in the gastric body and decreased inflammation in the antrum. Concerns have been raised that increased gastric inflammation may accelerate gastric gland atrophy (atrophic gastritis) and intestinal metaplasia—known risk factors for... 

In the mouse, whereas no evidence of H3 receptors was found in isolated gastric glands (Muller et al., 1993), in the whole stomach, (R)a-methylhistamine actually increased, and thioperamide decreased acid secretion, thus indicating a definite stimulatory role for H3 receptors in this species (Table 2). Apparently, this excitatory effect, which contrasts with the observations obtained in other models, was due to an inhibitory effect on somatostatin release from fundic D cells (Schubert et al., 1993 Vuyyuru and Schubert 1993). Also, an inhibitory effect on somatostatin secretion mediated by H3 agonists was observed in other species (rat and dog). However, contrarily to what might have been expected, in these species, the inhibitory effect on somatostatin is not followed by an increase in acid secretion, but it is instead followed by a decrease, owing to the predominant H3-mediated inhibition on the release of excitatory mediators (histamine, acetylcholine) from other sites (ECL, cholinergic nerve terminals)... 

Bado, A, Moizo, L., Laigneau, J.P, Lewin, M.J.M., 1992a. Pharmacological characterization of histamine H3 receptors in isolated rabbit gastric glands. Am. J. Physiol. 262, G56-G61. 

Muller, M.J., Padol, I., Hunt, R.H., 1993. Acid secretion in isolated murine gastric glands classification of histaminergic and cholinergic receptors. Gastroenterology 104 (Suppl), A151. 

Administration of muscarinic agonists, like parasympathetic nervous system stimulation, increases the secretory and motor activity of the gut. The salivary and gastric glands are strongly stimulated the pancreas and small intestinal glands less so. Peristaltic activity is increased throughout the gut, and most sphincters are relaxed. Stimulation of contraction in this organ system involves depolarization of the smooth muscle cell membrane and increased calcium influx. 

Gastric Glands with Chief and Parietal Cells... 

Omeprazole itself is not the active inhibitor of the H+, K+-ATPase, however. Rather, the transformation of omeprazole in acid is required to inhibit the H+, K+-ATPase in vitro and in vivo, whereas intact omeprazole is devoid of inhibitory action. Isolated H+, K+-ATPase is blocked by omeprazole only after the pretreatment of omeprazole with acid. Conversely, neutralization of the acid-secretory canaliculi of isolated gastric gland and parietal cell preparations by permeable buffers, which blocks the acid-catalyzed transformation of omeprazole, prevents inhibition of the enzyme. Furthermore, in-vivo blockade of acid secretion using an H2-receptor antagonist prior to omeprazole administration decreases the inhibitory potency of omeprazole, whereas the stimulation of acid secretion (e.g., by food intake) increases the potency. 

The last step in the omeprazole cycle (Scheme 1.2) finds support in the fact that the sulfide S is formed from omeprazole A in isolated gastric glands and in... 

Figure 4.1 Components of a gastric gland. The pit and the luminal surface are lined by surface mucous cells. The isthmus contains stem and progenitor cells and is enclosed by a sheath of myofibroblastic cells. Mucous neck cells are found in the neck, while chief and endocrine cells are present in the base of the gland. Parietal cells are actually scattered throughout the gland.

Figure 1.5. Histological changes in liver and stomach (Reprinted from Ito et al. 2003, with permission from Elsevier), (a) The liver 2 hour after p.o. gambierol at 140 pg kg , showing prominent congestions of sinusoidal capillaries at the periphery. P = portal veins. C = central vein, (b) Stomach alterations in the same conditions. Mucosa showed ulceration and erosion sporadically. E surface epithelial cells, G gastric glands, L lamina propria.

This corroborates the concept of Webster and Komarov, who wrote in 1933 (W6a) "... It seems more probable that pepsin, though, as Northrop states, itself a protein, is secreted by the gastric glands in a combination with a glycoprotein and possibly other proteins. ... 

G52. Glass, G. B. J., Pugh, B. L., and Wolf, S., Correlation of acid, pepsin and mucoprotein secretion by human gastric glands. J. Appl. Physiol. 2, 571-579 (1950). 

G73. Grossman, M. I., and Gillespie, I. E., Action of gastrin on the gastric glands. Intern. Congr. Physiol. ScL, 22nd Leiden, 1962 Part I, pp. 338-341. Elsevier, Amsterdam, 1962. 

C7. Crevier, M., and Belanger, L. F., Demonstration by electrophoresis and autoradiography of a sulfomucoprotein containing radiosulfate synthesized by the gastric glands of the rat. Compt. Rend. Soc. Biol. 148, 1530-1534 (1954). 

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