Biomedical subjects

M Petríková

Publications and source records attributed to M Petríková.

7 recordsLinked to original sources

PubMed1992

On the relationship between the inhibition of thrombin stimulated aggregation and thromboxane formation in isolated platelets treated with beta-adrenoceptor blocking drugs.

Thromboxane B2 (TXB2) formation in isolated, thrombin-stimulated rat platelets was time dependent and appeared after 5 s of incubation. Beta-adrenoceptor blocking (BAB) drugs inhibited thrombin-stimulated TXB2 formation in the following rank order of potency: metipranolol approximately alprenolol approximately propranolol > oxprenolol > practolol. Atenolol was ineffective in inhibiting TXB2 production in stimulated platelets. The inhibition of thrombin-stimulated TXB2 formation by BAB drugs correlated with their inhibitory effect on thrombin-stimulated platelet aggregation, arachidonic acid liberation from membrane phospholipids and with their membrane fluidization. The higher was the liposolubility of the beta-adrenoceptor blocking drugs investigated, the higher was their inhibition of stimulated TXB2 formation. Hydrophilic, selective atenolol and practolol revealed slight or no inhibitory effect on stimulated thromboxane production.

Adrenergic beta-Antagonists↗

PubMed1992

Dose-response aggregometry--contribution to the precise platelet function evaluation.

A method for the determination of blood platelet aggregability as the function of ADP concentration is described. Individual platelet aggregability was characterised by means of parameters of the sigmoidal relationship between the dose of the aggregating reagent and the aggregation curve amplitude. The method was applied to establish ADP-induced aggregability of various mammalian species. The aggregation curves of rabbit and rat platelets reached significantly lower maximum amplitudes than those of human and dog platelets. The eman concentration of ADP was significantly higher in dog platelets and the slope of the dose-response curve was significantly steeper in rat platelets compared to the other species studied. Some of the causes of individual intra-species ADP-induced aggregation variability revealed by means of dose-response aggregometry are discussed.

Animals↗

PubMed1992

Involvement of arachidonic acid and its metabolites in the inhibitory effect of beta-adrenoceptor blocking drugs on blood platelets.

Propranolol (PRO), alprenolol (ALP), metipranolol (MET) and oxprenolol (OXP) inhibited arachidonic acid (AA) liberation from membrane phospholipids, malondialdehyde (MDA) formation and thromboxane B2 (TXB2) production in stimulated platelets. The inhibition was dose-dependent and with slight variations followed the rank order of potency: PRO greater than or equal to ALP greater than or equal to MET greater than or equal to OXP. Atenolol (ATE) was without any inhibitory effect. Inhibition of the arachidonic acid pathway in stimulated platelets may significantly contribute to the antiaggregatory effect of beta-adrenoceptor blocking drugs.

Adrenergic beta-Antagonists↗

PubMed1992

Evidence on the role of three calcium pools in Ca-ionophore A23187-stimulated rat blood platelet aggregation.

The effect of Ca-ionophore A23187 on activation of rat blood platelets was investigated to elucidate the involvement of extracellular and intracellular Ca2+ ions. Platelet aggregation induced by 10 concentrations of the stimulus was studied in Ca-free medium as well as in the presence of EGTA and/or calcium. In Ca-free medium, A23187 induced platelet aggregation in a dose-dependent way; the mean effective concentration was 1.43 +/- 0.08 mumol/l. The stimulatory effect of ionophore was potentiated by addition of 0.01 and 0.1 mM calcium and inhibited when the calcium concentration was increased to 1 mmol/l. In the presence of EGTA, A23187-stimulated aggregation of isolated rat platelets was recorded only at a 10-times higher ionophore concentration and was then reduced to 30% in comparison with aggregation in Ca-free medium. The inhibitory effect of 1 mM EGTA was abolished by addition of 2 mM calcium. We suggest the participation of at least three calcium pools in the stimulation of rat platelets by A23187, i.e. the extracellular pool, the membrane-associated pool and the pool displacing calcium intracellularly.

Animals↗

PubMed1991

Atenolol, exaprolol and mast cell membranes.

Lipophilic exaprolol and hydrophilic atenolol differ in their interaction with mast cell membranes. Exaprolol, as compared with atenolol, significantly decreased 32P incorporation into, but increased arachidonic acid liberation from, membrane phospholipids. Moreover, exaprolol significantly decreased phosphate incorporation in compound 48/80 and ConA-PS treated cells and decreased thromboxane formation in stimulated cells. On the other hand, atenolol decreased significantly only arachidonate liberation from stimulated mast cells. These results corroborate to some extent the effect of exaprolol and atenolol on histamine liberation which correlates with their membrane perturbing properties.

Adrenergic beta-Antagonists↗

PubMed1991

[The role of prostaglandins in the effect of beta-blockers on stimulated blood platelets].

Atenolol, a selective beta-blocker, slightly potentiates the stimulated aggregation of platelets against dose-dependence. The drug potentiates similarly stimulated release of arachidonic acid, it does not influence the formation of malondialdehyde and the thromboxane B2 production in stimulated platelets. The non-selective beta-blocker propranolol inhibits in a dose-dependent way stimulated aggregation, the release of arachidonic acid, it reduces thromboxane B2 production in stimulated platelets. The authors revealed that the anti-aggregating action of beta-blockers is closely related to their ability to influence prostaglandin synthesis in stimulated platelets.

Adrenergic beta-Antagonists↗

PubMed1990

The effect of beta-adrenoceptor blocking drugs on histamine liberation, prostaglandin synthesis and phospholipid turnover in isolated mast cells stimulated with concanavalin A.

Exaprolol, metipranolol and propranolol decreased significantly histamine liberation, degranulation, 45Ca uptake and thromboxane B2 formation in isolated rat mast cells stimulated with concanavalin A and phosphatidylserine. Moreover, exaprolol and metipranolol decreased 32P incorporation into membrane phospholipids and metipranolol and propranolol reduced the liberation of arachidonic acid from membrane phospholipids of stimulated mast cells. Exaprolol significantly increased the arachidonic acid liberation from these cells. Possible mechanisms of interaction of beta-adrenoceptor blocking drugs with isolated mast cells are discussed.

Adrenergic beta-Antagonists↗