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Stomach acidification

Ionisation determines the partitioning of drugs across membranes. Unionised molecules can easily cross and reach an equilibrium across a membrane, while the ionised form cannot cross. When the pH is different in the compartments separated by the membrane the total (ionised + unionised) concentration will be different on each side. An acidic drug will become concentrated in a compartment with a high pH and a basic drug in one with a low pH. This is known as ion-trapping, and occurs in the stomach, kidneys, and across the placenta. Urinary acidification accelerates the excretion of weak bases, such as pethidine, while alkalinisation increases the excretion of acidic drugs, such as aspirin. As an example consider pethidine (pKa 8.6) with an unbound plasma concentration of 100 (arbitrary units). At pH 7.4 only 6% of the pethidine will be unionised so that at equilibrium the concentration of unionised pethidine in the urine will be 6 units. In urine at pH 6.5 only 0.8% of the pethidine will be unionised so that the total concentration in the urine will be 744 units. [Pg.33]

It has been suggested by Podesta et al. (650) that ambient C02 levels determine the amount of succinate and lactate excreted by intestinal helminths. A summary of the events which they propose lead to succinate accumulation in H. diminuta is provided in Fig. 5.7. There is considerable release of C02 in the post-prandial intestine of the rat host as the acidic chyme is passed into the duodenum and there is an acidification of worm tissues as the C02 diffuses in. The acidification is countered by worm secretion of H+ and by mobilisation of Ca2 + from the calcareous corpuscles (Chapter 4), thus releasing carbonate. The increased osmolality and greater HC03 concentration activate PEPCK, which favours succinate production over lactate. Succinate, being a dicarboxylic acid, is twice as effective as lactate in metabolic disposal of H+. With a decrease in passage of stomach chyme into the intestine, there would be a decrease in acid stress on the worms, accompanied by a concomitant decrease in tissue HC03 concentrations and osmolality, which would favour lactate production. [Pg.96]

The H+, K+-ATPase is a P-type ATPase proton (H+) pump responsible for acidification of the stomach. Inhibition of this pump by the tannin pentagalloylglucose may be the basis for the efficacy of Paeonia Radix (dried roots of Paeollia filciflom) for treatment of gastritis and peptic ulcers (Table 4.1). [Pg.124]

Gastric acid secretion can be inhibited by several mechanisms including acid in the stomach (pH 3 inhibits gastrin release), acid in the duodenum, the presence of fat in the pancreas, and hypertonic fluids or hyperglycemia. Somatostatin, a hormone produced by antral mucosal endocrine cells (D cells), inhibits the release of gastrin by directly inhibiting the parietal cells. Somatostatin is also present in other GI tissue and the pancreas. C cells, endocrine cells in the proximal small intestine, secrete secretin in response to mucosal acidification, which also decreases gastric secretion. [Pg.1223]

In this section, we describe the factors that influence the movement of water in and out of cells, an important feature of the life of both plants and animals. The following section discusses other transport phenomena that are critical to essential physiological processes, focusing on the asymmetrical distribution of certain transport proteins in epithelial cells. We will see how this permits absorption of nutrients from the intestinal lumen and acidification of the stomach lumen. [Pg.271]

A FIGURE 7-28 Acidification of the stomach lumen by parietal cells in the gastric lining. The apical membrane of parietal cells contains an H /K" ATPase (a P-class pump) as well as Cr and channel proteins. Note the cyclic transport across the apical membrane ions are pumped inward by the... [Pg.276]

Yamamoto, O., Matsunaga, Y, Haga, N., and Itoh, Z. (1994). Vagovagal inhibition of motilin-induced phase III contractions by antral acidification in dog stomach. Am. J. Physiol. USl, G129-134. [Pg.529]

Overdose with phencyclidine is dangerous. The basic principles of treatment are to maintain ventilation and to control seizures, blood pressure, and hyperthermia. Phencyclidine is secreted into the stomach, so removal of the drug may be hastened by activated charcoal or continual nasogastric suction. Phencyclidine is a weak base, and its renal elimination may be accelerated by urinary acidification. Treatment with antipsychotic drugs may be appropriate if psychotic symptoms follow the acute intoxication. The answer is (E). [Pg.295]

The most likely mechanisms, by which organic acids improve feed conversion ratio and animal health, include acidification, either of the feed or of the stomach, and/ or selective inhibition of pathogenic intestinal micro-organisms. They may also be... [Pg.40]

In the autumn of 1902 Cannon enlisted the help of Hilbert F. Day, a second-year medical student, to confirm his deductions about salivary digestion in the stomach. He and Day mixed 30 g of crackers known to be free of sugar with 100 ml of diluted, filtered saliva, and they found that in vitro at 38 C, 80% of the starch was turned to maltose in 7 minutes. They fed a thick mush of crackers mixed with distilled water to hungry cats, and at half-hour intervals they killed some of the animals, excised the stomachs, and separated the contents of the antrum from the contents of the body of the stomach. When they dried the contents and analyzed them for maltose, they found maltose in both samples, the ratio of antrum to body averaging 1 1.13 to 1 1.71. Cannon attributed the presence of sugar in the antrum to diffusion from the contents of the body. That seems unlikely. Cannon and Day did show that protein in the form of salmon mixed with crackers delayed acidification of gastric contents and increased starch hydrolysis. [Pg.320]

Riboflavin is delivered in form of free vitamin, or as its coenzymes, i.e. flavin mononucleotide (FMN) and adenine dinucleotide (FAD), which occurs mainly as a prosthetic group of flavoproteins. Release of coenzymes from flavoproteins by acidification in stomach and proteolysis, both gastric and intestinal, must precede the absorption. This hydrolysis also releases several percentages of covalently bound FAD from 8a-(peptidyl)riboflavins (Chia et al. 1978). Free riboflavin is physiologically preferred form of absorbed vitamin B2 (Daniel et al. 1983). The upper small intestine enzymes which catalyse reversible reactions of conversion nucleotides into riboflavin are located in the brush-border membrane of enterocytes (Figure 36.1). [Pg.624]

NaHCOg Sodium bicarbonate Oral antacid used to treat heartburn and acid stomach injected into blood to treat severe acidosis (acidification of the blood)... [Pg.391]

Inhibitors of the enzyme responsible for the acidification of the stomach are well known and equally well-advertised alleviators of heartburn. This enzyme is present in the parietal cells of the stomach and resembles the Na+/K+-ATPase. Instead of catalyzing the ATP-dependent exchange of Na+ and K+, the stomach acid pump excretes H+ into the lumen of the stomach in exchange forK+. [Pg.17]


See other pages where Stomach acidification is mentioned: [Pg.373]    [Pg.254]    [Pg.267]    [Pg.582]    [Pg.2995]    [Pg.547]    [Pg.414]    [Pg.1855]    [Pg.97]    [Pg.140]    [Pg.209]    [Pg.216]    [Pg.91]    [Pg.275]    [Pg.726]    [Pg.1437]    [Pg.2994]    [Pg.41]    [Pg.44]    [Pg.63]    [Pg.261]    [Pg.42]    [Pg.391]    [Pg.333]    [Pg.57]    [Pg.307]    [Pg.474]    [Pg.161]   
See also in sourсe #XX -- [ Pg.124 ]




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ACIDIFICATION

Stomach

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