Adenosine triphosphosphate (ATP), | |||
Adenosine cyclic 3’,5’-adenosine monophosphate, (cAMP), | |||
ATP transformation into ADP | |||
under physiological circumstances, | |||
under different pathological conditions, | |||
human gastric basal acid out, | |||
human gastric maximal acid output, | |||
human gastric antral ulcer, | |||
human duodenal ulcer, | |||
human jejunal ulcer, | |||
gastric acid secretion in pylorus-ligated rats, | |||
under different drug actions, | |||
ATP transformation into cyclic adenosine 3’,5’-AMP | |||
under physiological circumstances, | |||
under different pathological conditions, | |||
human gastric basal acid out, | |||
human gastric maximal acid output, | |||
gastric acid secretion in pylorus-ligated rats, | |||
gastric ulcer in pylorus-ligated rats, | |||
epinephrine ulcer model, | |||
stress ulcer model, | |||
Aspirin-induced mucosal damage | |||
Gastric H+ secretion, | |||
Gastric mucosal biochemistry | |||
During ulcer development | |||
During gastric mucosal protection produced by atropine | |||
During gastric mucosal protection by vitamin A and β-carotene | |||
Indomethacin ulcer model | |||
Biochemical backgrounds | |||
Cellular mechanisms, | |||
During gastric ulcer development, | |||
During gastric mucosal protection | |||
by atropine, | |||
by cimetidine, | |||
β-carotene, | |||
by vitamin A, | |||
Gastric mucosal cAMP vs gastric mucosal damage, | |||
Gastric mucosal cAMP vs, gastric mucosal protection, | |||
Prostaglandin system vs gastric mucosal protection by β-carotene, | |||
Reserpine ulcer model | |||
NaOH, NaCl, HCl and ethanol-induced gastric mucosal damage | |||
Time-sequence between the mucosal damage vs. introduction of chemical agents, | |||
Biochemical mechanisms vs. mucosal damage, | |||
Acid-dependent ulcer model vs. gastric mucosal biochemistry, | |||
Non- acid-dependent ulcer model vs. mucosal biochemistry, | |||
Gastric mucosal protection by PGI2 | |||
Gastric mucosal protection by β-carotene | |||
Gastric mucosal damage vs. oxygen free radicals | |||
Gastric mucosal protection vs. oxygen free radicals, | |||
Evidence-based medicine | |||
Problem-orientated medice, | |||
Human clinical pharmacology, | |||
Acute comparative clinical pharmacology in patients, | |||
Chronic atropine treatment in patients with duodenal ulcer | |||
Development of tolerance to atropine | |||
Development of drug tolerance to parasympatholytics, | |||
Pharmacological denervation phenomenon, | |||
Cytoprotection | |||
In patients with duodenal ulcer, | |||
In patients with gastric ulcer, | |||
In experimental circumstances, | |||
Prostaglandins, | |||
Retinoids, | |||
Small doses of atropine, cimetidine, | |||
Biochemical mechanisms of cytoprotection, | |||
Gastrointestinal mucosal biochemistry in patients, | |||
In gastric fundic mucosa with different gastric secretory responses, | |||
Biochemical and energetic gradients in mucosa of fundus vs. antrum vs. jejunum, | |||
Cholinergic ragulation of ATP-ADP transformation in the human gastric tissues | |||
Biochemistry of chronic ulcer in patients | |||
gastric antral ulcer, | |||
duodenal ulcer | |||
jenunal ulcer, | |||
exclusion of tissue hypoxia in the ulcerated mucosa, | |||
ATP-membrane ATPase- ADP system. | |||
First and second messenger systems | |||
Feedback mechanisms between Na+-K+-dependent ATPase and adenylate cyclase systems in intact gastrointestinal mucosal tissues |
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Under development of mucosal damage in different animal models | |||
Drug action on dependence of the funtional states of target organs | |||
Na+-K+-dependent ATPase vs. activity of membrane ATPase, | |||
Changes in the feedback regulations of cellular energy systems, | |||
Cellular energy systems | |||
„energy charge”[(ATP+0.5 ADP)/(ATP+ADP+AMP)] | |||
Na+-K+-dependent (transport) energy system | |||
Short review, | |||
In the gastrointestinal mucosa | |||
Gastric basal acid ouput in humans | |||
Gastric maximanl acid ouput in humans | |||
H+-K+-dependent ATPase | |||
Short review | |||
Adenylate cyclase system | |||
Short review, | |||
Isolated gastric mucosal cells (GMCs) | |||
Ethanol, | |||
Indomethacin, | |||
Helicobacter pylori | |||
Cellular damage at the levels of cell membrane mitochondion, DNA | |||
Stable cell lines | |||
Mouse cell myeloma cell line (Sp2/0-Ag14 cell line), | |||
Human hepatocellular carcinoma cell line ( Hep G2), | |||
„surgical” and „ chemical „ vagotomy | |||
Gastric acid secretion, | |||
Gastric mucosal protection, | |||
Biochemistry in the gastric mucosal biochemistry, | |||
Biochemistry of „use” and „disuse” in the rat gastric mucosa, | |||
Chronic atropine treatment | |||
In patients with chronic duodenal ulcer | |||
In rats | |||
Chronic treatment of rats with Neostigmine (choline) |