Thromb Haemost 1979; 42(04): 1164-1180
DOI: 10.1055/s-0038-1657012
Original Article
Schattauer GmbH Stuttgart

Study of Platelet Agglutination Induced by the Antibiotics of the Vancomycin Group: Ristocetin, Ristomycin, Actinoidin and Vancomycin

Zoltan Boda
The IInd Department of Medicine, University Medical School, 4012 Debrecen, Hungary, the Institute for Thrombosis Research, University of Oslo, Norway and the Research Group of Antibiotics, Hungarian Academy of Sciences, Lajos Kossuth University, 4012 Debrecen, Hungary
,
Nils Olav Solum
The IInd Department of Medicine, University Medical School, 4012 Debrecen, Hungary, the Institute for Thrombosis Research, University of Oslo, Norway and the Research Group of Antibiotics, Hungarian Academy of Sciences, Lajos Kossuth University, 4012 Debrecen, Hungary
,
Ferenc Sztaricskai
The IInd Department of Medicine, University Medical School, 4012 Debrecen, Hungary, the Institute for Thrombosis Research, University of Oslo, Norway and the Research Group of Antibiotics, Hungarian Academy of Sciences, Lajos Kossuth University, 4012 Debrecen, Hungary
,
Kalman Rak
The IInd Department of Medicine, University Medical School, 4012 Debrecen, Hungary, the Institute for Thrombosis Research, University of Oslo, Norway and the Research Group of Antibiotics, Hungarian Academy of Sciences, Lajos Kossuth University, 4012 Debrecen, Hungary
› Author Affiliations
Further Information

Publication History

Received 10 October 1978

Accepted 12 April 1979

Publication Date:
23 August 2018 (online)

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Summary

Four antibiotics which belong to the vancomycin group have been examined in respect of their effects on the factor VIII dependent platelet agglutination. A striking similarity between ristocetin and ristomycin was observed both in qualitative and quantitative terms, therefore ristomycin could be used to determine the so called ristocetin cofactor.

Actinoidin and vancomycin inhibited platelet agglutination induced by ristocetin or ristomycin in citrate-PRP or EDTA-PRP as well as in systems containing formaldehyde- treated platelets, but did not inhibit agglutination induced by bovine factor VIII.

All the four antibiotics caused plasma protein precipitation. Actinoidin was the least and vancomycin the most effective in this respect; ristocetin and ristomycin also possess this property, the effect of the latter is more considerable.

Actinoidin and vancomycin did not block the immediate increase in light absorbancy in aggregometer caused by the addition of ristocetin or ristomycin to fixed platelets at concentrations which totally inhibited platelet agglutination in the presence of protein cofactor. Inhibition of this »direct effect« of ristocetin and ristomycin was observed only at higher concentrations indicating that this effect may be unrelated to the agglutination.

According to our results with ristomycin derivatives the methylated carboxyl and the free phenolic hydroxyl groups may be of prime importance in the binding of ristomycin to the platelet membrane and/or to its protein cofactor. Similar data from other laboratories are confirmed and some new findings are offered.