Antihistaminic drug bromadryl and stimulated platelet aggregation

doi:10.1007/BF02007787

Paper

Antihistaminic drug bromadryl and stimulated platelet aggregation

Published Jun 1, 1994 · R. Nosál', V. Jančinová, M. Petríková

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Abstract

The H_1-receptor antagonist bromadryl dosedependently inhibited stimulated rat platelet aggregationin vitro. Bromadryl was 10 times more effective on the secondary aggregation of thrombin-stimulated platelets compared with its inhibition of ADP-stimulated primary platelet aggregation in plasma. The inhibition of aggregation was accompanied by a dose-dependent inhibition of thrombin-stimulated malondialdehyde formation and thromboxane B_2 production. The results indicate that bromadryl may interfere intracellularly with membrane phospholipid peroxidation and the arachidonic acid metabolism of stimulated platelets. Bromadryl, like other cationic amphiphilic drugs, may inhibit stimulated platelet functions by decreasing the stimulus-induced activation of phospholipase A_2. Our results support the possible interference of bromadryl with histamine as an intraplatelet messenger responsible for aggregation.

In Vitro Study

Study Snapshot

Bromadryl effectively inhibits stimulated platelet aggregation by interfering with histamine as an intraplatelet messenger responsible for aggregation.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

Antihistaminic drug bromadryl and stimulated platelet aggregation

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