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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 202, Supplement 684
The Joint Conference (FAMÉ 2011) of the LXXVth Meeting of the Hungarian Physiological Society, XVIth Meeting of the Hungarian Society of Anatomists, Experimental Section of the Hungarian Society for Experimental and Clinical Pharmacology and Hungarian Society for Microcirculation and Vascular Biology
6/8/2011-6/11/2011
Pécs, Hungary


IN VITRO COMPARISON OF PLATELET AGGREGATION INHIBITORY EFFECT OF ACETYLSALICYLIC ACID AND METAMIZOLE IN BLOOD SAMPLES OF HEALTHY SUBJECTS
Abstract number: P65

Papp1 J., Vamos2 Z., Sandor1 B., Toth1 A., Rabai1 M., Kenyeres1 P., Cseplo2 P., Koller2 A., Toth1 K.

Aims: 

Several clinical studies proved the effectiveness of platelet aggregation inhibition in the treatment and prevention of acute cardiovascular events. Orally administered acetylsalicylic acid (e.g. Aspirin) is the most commonly used drug for that, though some patients show laboratory resistance for the treatment. Metamizole (e.g. Algopyrin) is a widely known painkiller and antifebrile drug that can be administered intravenously also. It is not used for platelet inhibition. Effect of platelet aggregation inhibition of acetylsalicylic acid (ASA) and metamizole (MET) was compared in our in vitro study.

Methods: 

Different concentrations (6, 12 és 25 mg/ml) of ASA and MET solutions were added to blood samples obtained from healthy subjects (n=10). After one hour of incubation platelet aggregometry was performed using epinephrine and adenosine-diphosphate inductors by Carat TX4 optical aggregometer. Inhibition of platelet aggregation was considered to be effective if less than 40% of the maximal change in light transmission intensity due to total platelet aggregation could be induced.

Results: 

Platelet aggregation induced by epinephrine was significantly lower, consequently effective, in all examined ASA and MET concentrations. There were no significant differences in aggregation in equivalent doses of ASA and MET. Examining the dose-effect curve of MET we found out, that compared to the calculated plasma concentration (300 mg/ml) of the intravenously administered usual MET dose (1g/2ml), used as a painkiller and antifebrile, platelet aggregation was effectively inhibited in very low concentrations (1–2 mg/ml) during the in vitro measurements.

Conclusions: 

Short term inhibition of platelet aggregation of MET did not differ significantly from ASA. When using MET intravenously probably less resistance will occur than in case of ASA therapy. In case of acute ischemic cardiovascular events, when orally administered ASA for platelet inhibition can not be used for certain reasons, intravenously administered MET can be considered as a therapeutic alternative.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 202, Supplement 684 :P65

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