Drugs online research references
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The effect of omeprazole, a clinically used proton pump inhibitor, alone or in combination with clarithromycin was evaluated against Mycobacterium avium, Mycobacterium intracellulare and Mycobacterium tuberculosis, using a human alveolar macrophage model of infection. Omeprazole exhibited no significant effect on the growth of the two M. avium complex strains or on the mycobactericidal activity of clarithromycin against them. In contrast, omeprazole significantly promoted the growth of Mycobacterium tuberculosis and the anti-mycobacterial activity of clarithromycin against it in human alveolar macrophages. It was speculated that intracellular acidic milieu around M. tuberculosis might be one reason for the lower activity of clarithromycin in the treatment of human tuberculosis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10612733&dopt=Abstract
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Am J Physiol. 1983 Jul;245(1):G64-71.
Differentiation among inhibitory actions of omeprazole, cimetidine, and SCN- on gastric acid secretion.
Wallmark B, Jaresten BM, Larsson H, Ryberg B, Brandstrom A, Fellenius E.
The action of the substituted benzimidazole omeprazole (H 168/68) was studied in three different in vitro preparations: the isolated guinea pig gastric mucosa, isolated intact and permeable rabbit gastric glands, and hog fundic microsomal membrane vesicles containing H+-K+-ATPase. The effects of omeprazole were compared with those of cimetidine and thiocyanate (SCN-). Under all the conditions studied, cimetidine only counteracted histamine-induced acid secretion, consonant with its H2-receptor antagonism. In contrast, omeprazole and SCN- were found not only to inhibit histamine-induced secretion but also basal acid formation and acid formation induced by dibutyryl cAMP and a high cell medium concentration of K+. Moreover, acid production induced by ATP in permeable gastric glands was antagonized by omeprazole and SCN-, whereas cimetidine was without effect. The interaction pattern of omeprazole and SCN- was differentiated by studies using the weak base antipyrine in the isolated mucosal preparation, where it was found that antipyrine could reverse the inhibition induced by SCN- but not that of omeprazole. Furthermore, omeprazole was found to inhibit the isolated H+-K+-ATPase, whereas cimetidine or SCN- was without effect. In the isolated mucosal preparation omeprazole caused an increase in K+ secretion rates in parallel with the inhibition of acid formation. This was in contrast to what was observed for cimetidine and SCN-, which exhibited no such increased K+ secretion. The results obtained from intact mucosa and isolated glands are in agreement with the ability of omeprazole to inhibit the isolated H+-K+-ATPase and thus provide evidence of a novel mechanism of action for this inhibitor.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6307064&dopt=Abstract
note: kwd match prilosec online literature
Dig Dis Sci. 1994 Jan;39(1):169-76.
Effect of proton pump inhibitor, omeprazole, on expression of rat parietal cell specific carbohydrate antigen, type 2 chain N-acetyllactosamine.
Usumoto R, Okada Y, Tsuji T.
First Department of Internal Medicine, Okayama University Medical School, Japan.
The effect of a proton pump inhibitor, omeprazole, on the rat gastric mucosal expression of carbohydrate antigens was studied. Type 2 chain N-acetyllactosamine was detected specifically on the apicocanalicular cell membranes of parietal cells. Pretreatment of rats with omeprazole profoundly suppressed the antigen expression, which followed the inhibition of gastric acid secretion. When omeprazole was discontinued, the antigen was reexpressed, which preceded the restoration of acid secretion. The antigen-negative tissues became antigen-positive when they were desialylated. Gastric membrane vesicles from the normal and omeprazole-treated rats were antigen-positive and -negative, respectively. SDS-PAGE revealed that a glycoprotein with an apparent molecular weight of 64-78 kDa carried type 2 chain N-acetyllactosamine. In the omeprazole-treated rats, the same molecular weight glycoprotein was positively immunostained only after desialylation. We concluded that: (1) the expression of type 2 chain N-acetyllactosamine was closely correlated with gastric acid secretion, and (2) the inhibition of acid secretion was accompanied by the sialylation of the parietal cell membrane glycoprotein.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8281853&dopt=Abstract
note: kwd match prilosec online literature
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