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T Jávor

Publications and source records attributed to T Jávor.

At least 37 records · Page 2Linked to original sources
PubMed1990

Effects of a novel Hungarian antacid containing Al and Mg (Tisacid) on mucosal prostaglandin generation and oxygen free radicals in normal rats.

A new patented chemical agent (Al-Mg-hydroxy-carbonate; acid-binding capacity greater than 30 mmol/g) was produced by our work-team. After our preliminary pharmacological and some prospective, randomized, multicentre, controlled clinical studies, this antacid was registered (Tisacid tablet and suspension; Alkaloida, Hungary). A cumulative ulcer healing rate of 80-85% was proved by Tisacid monotherapy applied in low doses (from 80 to 160 mmol/day) in patients with duodenal ulcer. The aims of this study were: (i) to determine the role of different antacids on the genesis of mucosal prostaglandins (PGs) (PGE2 and 6-keto-PGF1 alpha) in normal rats; (ii) to evaluate the effects of indomethacin pre-treatment (20 mg/kg b.w.,s.c.) on the Tisacid-induced alterations of gastric mucosal PG-contents; (iii) to analyse the generation of oxygen free radicals and lipid peroxidation in the rat oxyntic mucosa by the application of different doses of Tisacid (activities of CAT, GSH-px and SOD, contents of MDA and red. GSH). It was found that: Tisacid has a potent gastroproprotective effect in gastric mucosa, via (a) an increase in the mucosal levels of PGs, and (b) a scavenging-like effect in normal rat gastric mucosa. It is concluded that the gastroprotective effect of Tisacid appears because of the following: (i) excellent acid-neutralizing capacity; (ii) mucosal generation of PGs (PGE2 and PGI2); (iii) free radical scavenging; (iv) its possible activity as a Ca-antagonist (Mg-containing compound).

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Pattern recognition in evaluation of haemorheological and haemodynamical measurements in the cardiological diagnostics.

The non-invasive differential diagnosis of ischaemic heart disease (IHD) and acute myocarditis or secondary cardiomyopathy following myocarditis can be difficult on the basis of the complaints, resting and exercise ECG and nuclear cardiological tests. 92 patients (mean age: 46 years) in the first step and 100 patients (mean age: 44 years) in the second step all with heart troubles, were examined. Besides determination of the routine parameters, nuclear haemodynamical and haemorheological measurements were carried out. Then each group of the patients was classified into 4 subgroups: 1) myocardial infarction /n:9/, 2) IHD /52/, 3) myocarditis /28/, 4) chronic cor pulmonale (CCP) /3/ subgroups in the first group and 1) normal /n:20/, 2) IHD /50/, 3) myocarditis /16/, 4) chronic cor pulmonale /14/ subgroups in the second group. The patients were reclassified by our multivariate pattern recognition algorithm (PRIMA). The average effectiveness of our method was over 80%, the recognition abilities for the subgroups (classes) ranged between 71 and 100%. An analysis of the discrimination power of the properties has made it evident that the haemorheological features were more characteristic than the haemodynamic ones in distinguishing the two differential-diagnostically critical groups. Our results show that our multivariate statistical method can be useful for the computer-aided decision in cardiological diagnostics.

Acute Disease↗
PubMed1989

Similarities and differences in the cytoprotection induced by PGI2 and beta-carotene in experimental ulcer.

UNLABELLED: It was earlier known that PGI2 and beta-carotene have a cytoprotective effect, but the similarities and the differences of their mechanisms were not clear. The gastric mucosal lesions were produced by ig. administration of 1 ml 96% ethanol and 1 ml 0.6 N HCl in rats. The 5 and 50 micrograms/kg dose of PGI2 and the 1 and 10 mg dose of beta-carotene was given 30 min. earlier. The animals were sacrified 1, 5, 15, 30 and 60 minutes after the administration of the necrotizing agent. The number and the severity of gastric mucosal lesions were noted. It was found that the number and the severity of gastric ulcers were dose-dependently decreased in each model after using either PGI2 or beta-carotene. The inhibiting effect of PGI2 appeared in the first last 15 minutes while beta-carotene was effective from 15 to 60 minutes. CONCLUSION: The mechanism of the cytoprotection induced by PGI2 differ from the beta-carotene induced one. PGI2 plays a part in the earlier vascular phase. beta-carotene modulates the repair mechanisms.

Animals↗
PubMed1989

A pharmacological approach to cellular mechanisms of PGI2-induced gastric cytoprotection on ethanol-induced gastric mucosal damage in rats.

The aims of this study were as follows: 1. to analyse the effects of drugs with different subcellular mechanisms on the PGI2-induced gastric cytoprotection in a non acid dependent (ethanol-induced) gastric ulcer model; 2. to identify the affinity and intrinsic activity curves on the PGI2-induced gastric cytoprotection; 3. to evaluate the main cellular mechanisms of PGI2-induced gastric mucosal defence. The observations were carried out on both sexes of CFY-strain rats, weighing 180 to 210 g. The gastric mucosal damage was produced by intragastric administration of 96% ethanol. The animals were killed at 1 hr after administration of ethanol, and the number and severity of gastric mucosal lesions (ulcers) was noted. Atropine, actinomycin D, cimetidine, mannomustine, dinitrophenol, epinephrine, pentagastrin, histamine, ouabain, tetracycline were given intraperitoneally (in different doses) at 30 min before administration of ethanol. The effects of these drugs were tested on the PGI2-induced (5 micrograms/kg was given intragastrically) gastric cytoprotection. It has been found that: 1. atropine, actinomycin D, cimetidine, epinephrine, ouabain, tetracycline and mannomustine inhibited the PGI2-induced gastric cytoprotection; 2. histamine, pentagastrin and 2,4-dinitrophenol enhanced the PGI2-induced gastric cytoprotection; 3. the molar concentrations of these drugs modifying the PGI2-induced gastric cytoprotection differed significantly. It has been concluded that: 1. the drugs stimulating or inhibiting the cell functions are capable to modify the extent of PGI2-induced gastric cytoprotection; 2. different subcellular mechanisms (oxidative phosphorylation, increased synthesis of proteins, ribonucleic and deoxyribonucleic acids, modifications of membrane-bound ATP-dependent energy systems) are involved in the development of PGI2-induced gastric cytoprotection.

Animals↗
PubMed1989

Free radicals and their interpretations.

Oxygen free radicals can be blamed for evoking gastric mucosal damage, because of the protective effect of some lipid soluble free radical scavengers (vitamin A related compounds, Vitamin E). Direct determination of free oxygen radicals related chemical entities in the gastric tissue during ulcerogenesis yielded controversial results. Aluminum antacid compound together with acid binding property exhibited cytoprotection too, elevating the tissue PGE2 level substantially. Magnesium containing antacid according to our model experiments on red blood cells damage by free radicals, is capable to bind free radicals as well as to counteract with the dangerous intracellular calcium accumulation. It has been concluded that aluminum-magnesium antacid has a cytoprotective effect via: 1. acid binding; 2. prostaglandin generation; 3. free radical scavenging; 4. calcium antagonist activity.

Aluminum Hydroxide↗
PubMed1989

Effect of ionic milieu to the free radicals generated by phenizine methosulphate (PMS).

The effect of free radicals generated by PMS was studied for membrane damage in the presence of different ions in the erythrocyte model. The degree of membrane damage depended on the quality of ionic composition in the incubation medium. We supposed that the degree of membrane damage depends on the average life and concentration and/or reactivity of the free radicals generated. For control of this supposition free radicals were generated by PMS in the presence of Sodium-di-thionite in isosmotic, waterly systems with different ionic composition. At different time intervals the concentration of free radicals was measured by the ESR method. It seams that concentration of radicals depends on the qualitative composition of ionic milieu. The increase of the average life of free radicals generated by PMS is accompanied by decrease in their reactivity. This is reflected by a moderate membrane damage.

Electron Spin Resonance Spectroscopy↗
PubMed1989

Cellular energy status of the gastric mucosa and gastric mucosal prevention by vitamin A in indomethacin-treated rats.

To evaluate the cellular energy status of gastric mucosa during the development of gastric mucosal damage and its prevention by application of a cytoprotective scavenger (vitamin A) in rats treated with indomethacin, the tissue levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and lactate were measured enzymatically, while the concentration of cyclic adenosine monophosphate (cAMP) was measured by radioimmunoassay, 4 h after the treatment with indomethacin and vitamin A simultaneously. It was found that a) the tissue levels of ATP, cAMP, AMP and the ratio of ATP/ADP were increased dose-dependently in the gastric mucosa in connection with the development of gastric mucosal prevention produced by vitamin A, b) the tissue level of ADP was decreased dose-dependently by vitamin A in indomethacin-treated rats, and c) the value of "energy charge" and the ratio of the ATP-ADP was unchanged during the vitamin A treatment in indomethacin-treated rats. The presence of tissue hypoxia could not be proved either in the development of indomethacin-induced gastric mucosal damage nor in the prevention of gastric mucosal damage by vitamin A.

Adenosine Diphosphate↗
PubMed1989

Effect of atropine, PGF2 alpha and cimetidine on the beta-carotene induced cytoprotection in ethanol-treated rats.

The aim of the study was to evaluate the influence of atropine, PGF2 alpha and cimetidine on the gastric cytoprotective effect of beta-carotene. Mucosal damage was produced by intragastric (i.g.) addition of 96% ethanol in CFY-strain rats of both sexes weighing 180-220 g. Gastric cytoprotection caused by i. g. pretreatment with 1.0 mg/kg beta-carotene 30 minutes before ethanol administration, was observed after 1 hour. Atropine (0.5 mg/kg), cimetidine (50 mg/kg) and PGF2 alpha (200 micrograms/kg) were given intraperitoneally (i.p.) 30 minutes before ethanol administration with and without beta-carotene and the changes in the number and severity of the gastric ulcers were detected. PGF2 alpha did not influence the gastric cytoprotective effect of beta-carotene meanwhile it was inhibited by atropine and markedly by cimetidine. Deleterious effect of cimetidine on the beta-carotene-induced cytoprotection may be explained perhaps by the adverse effect of the two compounds on ATP-cAMP transformation hereby counteracting one another, but more data are needed to the better understanding of drug interactions relating to mucosal cytoprotection.

Animals↗
PubMed1989

Drug metabolism in drug-induced liver diseases: pathogenetic role of active metabolites.

Three cases with drug-induced liver diseases (hepatitis caused by hydralasine, steatosis caused by methimazole, choletasis caused by birth control pill) were investigated with respect to their drug metabolising ability. Clinical diagnoses were based on the exclusion of other pathogenetic factors, on histological findings of liver biopsy specimens and on the clinical chemical tests. Investigation of biotransforming ability was carried out using test materials (menthol loading, antipyrine, sulfadimidine, caffeine, indocyanine green kinetics) and measurement of D-glucaric acid excretion. In all cases the results show a defective capacity in some respect of drug metabolism. Possible pathogenetic role of reactive metabolites is discussed in the pathomechanism of genesis of drug-induced liver diseases.

Adult↗
PubMed1989

In vitro method for measurement of free radical effects: effect of PMS (phenazine methosulphate) on red blood cell membrane.

The aim of this study was to elaborate a simple in vitro model for rapid and quantitative measurement of free radical effects. Free radical generating characteristics of PMS were measured in the case of red blood cell (RBC) membrane. The mechanism of free radical action was investigated in MgCl2, CaCl2, BaCl2 and in Verapamil HCl medium. The most important result of the investigations is as follows: Membrane damage of RBC provoked by the mechanism of free radical generation of PMS is proportional to the intracellular K+-efflux and to the extracellular Na+-influx. The PMS dependent K+-efflux in a NaCl containing medium in the presence of CaCl2 increases significantly, while it remains unchanged in MgCl2 medium. The PMS dependent K+-efflux and Na+-influx were considerably decreased by Verapamil HCl in NaCl containing solution. We have come to the conclusion that new, non-selective pores are formed in the membrane. The measure of the damage increases in the presence of Ca2+ions and decreases in the medium containing Verapamil HCl.

Barium↗
PubMed1989

The free radical mechanisms in beta-carotene induced gastric cytoprotection in HCl model.

The aims of our experiments were to clear up the possible correlations between the free radical mechanisms and the gastric cytoprotection of beta-carotene on HCl-induced gastric mucosal lesions. The beta-carotene was intragastrically given in doses of 1 and 10 mg/kg and 30 min. later 1 ml 0.6 N HCl was given to provoke the mucosal damage. After 1, 5, 15, 30 and 60 min. the animals were sacrificed. The number and severity of gastric mucosal lesions were calculated. The superoxide dismutase (SOD), glutathion peroxidase (GPX), catalase (CAT) activity and the malondialdehyde (MDA) and reduced glutathion (GSH) contents were determined from the gastric mucosa of rats. It was found that 1. beta-carotene was able to reduce the number and severity of ulcers only after 30 min.; 2. the CAT activity was decreased at 60 min. by carotene; 3. the GPX activity became dissimilar in the different groups after 15 min; 4. the changes of GSH were found to be similar ones; 5. the SOD activity was lower during the cyto-protection; 6. the MDA level remained practically unchanged. It has been concluded that 1. the free radicals are the consequences of the development of gastric ulcer and cytoprotection; 2. the scavenger character of beta-carotene is involved in its cytoprotective effect.

Animals↗
PubMed1989

A controlled multicentre therapeutic trial to determine the efficacy of a novel antacid (AI-Mg-hydroxy-carbonate) in duodenal ulcer.

Tisacid (a new, modern Hungarian AI-containing antacid) with a high acid-neutralizing capacity (greater than 26.8 mmol/g) also enhances gastric mucosal defense mechanisms (prostaglandin-dependent gastroprotection). A simple-blind, prospective, randomized, parallel multicentre clinical trial has been performed on both the clinical efficacy and possible side-effects of Tisacid monotherapy (AI-Mg-hydroxy-carbonate) on informed patients suffering from active duodenal ulcers. The four study groups were as follows: Group A: 3 g/day of Tisacid (acid-neutralizing capacity = 78 mmol, n = 85), Group B: 6 g/day of Tisacid (acid-neutralizing capacity = 156 mmol, n = 88), Group C: 12 g/day of Tisacid (acid-neutralizing capacity = 312 mmol, n = 68), Group D (as control): 1.0 g/day cimetidine (n = 91). The total number of patients was 332. It was found that the new Hungarian antacid compound (both tablet and suspension) can essentially accelerate the healing rate of duodenal ulcers; the cumulative healing rate of ulcers and the decrease of complaints can be achieved equally by relatively low doses of Tisacid monotherapy and cimetidine alone; and there were no essential differences between the clinical potency and side-effects of Tisacid tablets or the suspension.

Adolescent↗