Mucosa gastric

Histamine AND histamine antagonists). It is formed from histidine by the enzyme L-histidine decarboxylase. In the periphery, histamine is stored ia mast cells, basophils, cells of the gastric mucosa, and epidermal cells. In the CNS, histamine is released from nerve cells and acts as a neurotransmitter. The actions of histamine ate terrninated by methylation and subsequent oxidation via the enzymes histamine-/V-methyltransferase and monoamine oxidase. 

Permeation enhancers are used to improve absorption through the gastric mucosa. Eor example, oral dehvery of insulin (mol wt = 6000) has been reported from a water-in-oH- emulsion containing lecithin, nonesterified fatty acids, cholesterol [57-88-5], and the protease inhibitor aprotinin [9087-70-1] (23). 

Delivery systems that respond to changes in pH have been known to the pharmaceutical industry for more than a century. The pH-sensitive enteric coating is probably the oldest controUed-release technology. Unna introduced an enteric tablet coating based on keratin in 1884 (108). Enteric coatings are used primarily to protect the gastric mucosa from local irritation or to ensure that tablets do not dissolve until they reach the intestine. 

Histamine is a substance present in various tissues of die body, such as die heart, lungs, gastric mucosa, and skin (Pig. 36-1). The highest concentration of histamine is found in die basophil (a type of white blood cell) and mast cells diat are found near capillaries. Histamine is produced in response to injury. It acts on areas such as die vascular system and smooth muscle, producing dilatation of arterioles and an increased permeability of capillaries and venules. Dilatation of die arterioles results in localized redness. An increase in die permeability of... 

Pernicious anemia Anemia resulting from lack of secretions by the gastric mucosa of the intrinsic fador essential to the formation of RBCS and the absorption of vitamin B ... 

The proton pump inhibitors suppress gastric acid secretion by blocking the final step in the production of gastric acid by the gastric mucosa... 

A chronic toxicity study for DOSS was performed using beagle dogs [72]. The dogs showed no toxic effects over a one-year period. Not even an effect on gastric mucosa was found (in contradiction to an earlier study [101] see also [102]). 

Epidemiologic studies of the macroenvironment focused on the diet and the long incubation period have led us to postulate that long-lasting disturbances in the normal gastric mucosa may determine the final outcome of the neoplastic transformation W. This explains the present interest in precursor lesions rather than in cancer itself. We, therefore, need to scrutinize the gastric microenvironment and attempt to point out the components that may be relevant to neoplasia. The microenvironment could be considered to be determined by three basic elements ... 

The nitrite results from reduction of nitrate by bacteria abnormally present in the gastric mucosa and the gastric cavity. The bacteria grow situ because the pH is elevated as a result of loss of HCl secretion secondary to the loss of parietal cells and their replacement by intestinal-type epithelium. Parietal cells are lost as a result of chronic atrophic gastritis. What... 

Hall et al. [62] identified in a separate study the same glycoprotein in H,K-ATPase vesicles isolated from porcine gastric mucosa. A stoichiometric ratio of 1.2 1.0 was found for the deglycosylated protein (35 kDa)/catalytic 94-kDa protein. Furthermore, compelling evidence that this glycoprotein is the H,K-ATPase p subunit was provided by N-terminal sequence analysis of three protease V8-obtained peptides of the 35-kDa core protein. These peptides showed 30% and 45% homology with the Na,K-ATPase pi and pi subunit, respectively. 

Studies on patients with established gastric cancer have shown decreased levels of SOD in whole blood and also gastric mucosa (Oka et al., 1990b Lan-Kai-Wei et al. ... 

Davies, G.R., Simmonds, N.J., Stevens, T.R.J., Grandison, A. and Rampton, D.S. (1991). Enhanced production of reactive oxygen species by gastric mucosa infected with Helicobacter pyirri. Gut 32, A564. 

Iwata, F., Joh, T., Kawai, T., Kasugai, K., Itoh, M. and Takeuchi, T. (1992). Role of endogenous EDRF in ischaemia-reperfiision injury of rat gastric mucosa. Gastroenterology 102, A89. 

Kishi, A., Yoshikawa, T., Naito, Y., Ando, T., Yasuda, M., Tsujigiwa, M., Tomii, T., Takahashi, S., Tas i, M., Takano, H. and Kondo, M. (1990). Evaluation of superoxide dismu-tase activity in the gastric mucosa of chronic peptic ulcer patients. Gastroenterology 98, A68. 

Kvietys, P.R, Twohig, B., Danzell, J. and Specian, RD. (1990). Ethanol-induced injury to the rat gastric mucosa. Role of neutrophil and xanthine oxidase-derived radicals. Gastroenterology 98, 909-920. 

Loguercio, C., Romano, M., Taranto, D., Nardi, G., Di Sapio, M. and Del Vecchio Blanco, C. (1990). Regional variations in tissue levels of sulphydryl compounds in the human gastric mucosa effect of ethanol. Gastroenterology 98, A81. 

Oka, S., Ogino, K., Hobara, T., Yoshimura, S., Okazaki, Y., Takemoto, T., Kato, N., lida, Y. and Uda, T. (1990b). An immunohistochemical study of copper, zinc-containing superoxide dismutase detected by a monocloncal antibody in gastric mucosa and gastric cancer. Histopathology 17, 231-236. 

Von Ritter, C., Oostuizen, M.M.J., Lambrechechts, H., Hunter, S., Svensson, E G. and Hinder, R.A. (1986). Free radical scavengers decrease reperfusion damage of the gastric mucosa in baboons. Gastroenterology 90, A1682. 

Whittle, B.J.R, and Lopez-Belmonte, J. (1992). Protection and injury of the rat gastric mucosa by nitric oxide donors. Gas-troenterolcgy 102, A188. 

---