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Biomedical subjects

A Kohút

Publications and source records attributed to A Kohút.

At least 37 records · Page 2Linked to original sources
PubMed1992

The influence of prolonged cimetidine administration on serum gastrin levels and gastric acid secretion in rats.

The correlation between serum gastrin levels and gastric acid secretion during 4 weeks of cimetidine administration (once daily) was investigated. Serum gastrin levels and gastric acid secretion were estimated on the 7th, 14th, 21st and 28th day after cimetidine administration (25 mg.kg-1, intragastrically). At the mentioned time intervals gastric acid secretion stimulated by histamine and pentagastrin was also studied. It was found that on the 14th and 21st day after cimetidine administration serum gastrin levels were significantly elevated. Basal gastric acid secretion after cimetidine administration was significantly decreased at all the observed time intervals. Histamine-stimulated gastric acid secretion was increased on the 14th, 21st and 28th day after cimetidine administration. Hypoacidity was not followed at all time intervals by hypergastrinaemia (only on day 14 and 21 after cimetidine).

Animals↗
PubMed1991

Effect of stobadine on indomethacin- and ethanol-induced stomach lesions and gastric secretion.

Stobadine was found to inhibit the ulcerogenic activity of indomethacin in relation to the dose but was ineffective against the direct necrotizing action of ethanol. It also inhibited gastric acid secretion when administered intraduodenally. Although stobadine is considered to be a scavenger of free radicals, our results indicate that, under the given experimental conditions, it is rather the inhibition of gastric acid secretion that is responsible for its antiulcerogenic effect. The preliminary results do not allow the exclusion of other mechanisms for explaining its antiulcerogenic effect.

Animals↗
PubMed1991

Antiulcerogenic effect of pentacaine, chlorpromazine and stobadine on ethanol- and indomethacin-induced stomach lesions in rats.

The aim was to compare the antiulcerogenic effect of pentacaine, chlorpromazine and stobadine on indomethacin- and ethanol-induced stomach lesions in rats. Pentacaine effectively inhibited the formation of ethanol lesions, but in the given dose and under the given experimental conditions it was ineffective against indomethacin-induced damage. Chlorpromazine and stobadine effectively inhibited indomethacin erosions, but did not affect ethanol lesions significantly. The similarity of the effect of chlorpromazine and stobadine as compared with pentacaine, in the two stomach injury models, allows the assumption that stobadine has properties typical for an indirectly acting antiulcerogenic substance. This newly discovered property of stobadine extends the possibilities of its utilization to a further set of indications.

Animals↗
PubMed1991

Effect of chlorpromazine on ulcer formation by indomethacin in histamine- and insulin-stimulated rats.

The effect of chlorpromazine on ulcer formation by indomethacin and on total gastric secretion and gastric acid secretion was studied in rats. Secretion and ulceration were evaluated under basal conditions and after the administration of histamine or insulin, i.e. substances stimulating gastric acid secretion. The authors confirmed that chlorpromazine inhibits basal secretion and found that it also inhibits histamine- and insulin-stimulated gastric secretion, in correlation to the dose. It also strongly inhibits the formation of stomach lesions caused by indomethacin under basal conditions and after pretreatment with histamine (3 and 10 mg/kg) and insulin (0.3 IU/kg). Chlorpromazine did not inhibit lesions formed after combining indomethacin with insulin in a dose of 3 IU/kg. The results show that although chlorpromazine inhibits both basal and centrally or peripherally stimulated gastric secretion, its effect on stomach lesions caused by indomethacin is not uniform. Pretreatment with insulin in a dose of 3 IU/kg demonstrates that indomethacin-induced stomach lesions are markedly potentiated by this dose of insulin and are not dependent on gastric secretion only. The inability of chlorpromazine to inhibit these lesions gives the evidence that other--probably central--mechanisms play a role in their development.

Animals↗
PubMed1989

[Age-dependent effect of non-steroidal anti-inflammatory agents on the phagocytic activity of leukocytes in mice].

In experiments on mice of five different age groups (representing important stages of ontogenetic development) the phagocytic activity of polymorphonuclear leukocytes in peripheral blood was studied after short-term administration of phenylbutazone, indomethacin, ibuprofen, and diclofenac sodium. In six-week-old mice (period of sexual maturation) administration of phenylbutazone and indomethacin resulted in statistically significant increase of phagocytic activity. After administration of phenylbutazone to 18-month-old mice (old), phagocytic activity was reduced. In the groups of 3-week-old and 3- and 12-month-old mice phenylbutazone and indomethacin did not significantly affect phagocytic activity. Administration of ibuprofen resulted in statistically significant decrease of phagocytic activity of leukocytes in three age groups, i.e. in 3-week-, 6-week- and 18-month-old rats. In the other two age groups ibuprofen failed to be effective. No effect of diclofenac sodium on phagocytic activity of leukocytes could be established in comparison with the control group of mice in any of the age groups studied. The finding that phagocytic activity of leukocytes can be diminished even after short-term administration of ibuprofen is considered important, since it is currently one of the most frequently used anti-inflammatory drugs.

Aging↗
PubMed1988

Comparison of the ulcerogenicity of indomethacin and the gastric secretion in verapamil-treated rats.

The authors studied the effect of different doses of verapamil on the ulcerogenic activity of indomethacin (20 mg.kg-1) in rats. This was compared with the effect of verapamil on total gastric juice secretion, the amount of acid and the pH. It was found that, as distinct from total secretion and the amount of HCl, which verapamil reduced in correlation to the dose, ulcerogenicity after indomethacin was inhibited the most by a dose of 10 mg.kg-1 verapamil. Larger doses (20 and 30 mg.kg-1) did not increase the anti-ulcerogenic effect any further. This implies that verapamil-induced inhibition of the ulcerogenicity of indomethacin is not related directly to inhibition of total and acid gastric juice secretion.

Animals↗