Key result
Penicillin G inhibits ADP, collagen, or thrombin-induced platelet aggregation, release, and adherence to collagen in human, rabbit, and pig platelets.
Why the study?
Does Penicillin G inhibit platelet aggregation and adherence in human and animal platelets?
Does Penicillin G inhibit platelet aggregation and adherence in human and animal platelets?
High concentrations of Penicillin G inhibit platelet aggregation and adherence, which may explain alterations in platelet function during massive or local penicillin therapy.
Answers are grounded in this paper and cite their sources.
May alter hemostasis during high-dose penicillin therapy; leaves open in vivo clinical relevance.
Penicillin G (1000–8000 units/ml) inhibits ADP, collagen or thrombin-induced platelet aggregation and the release reaction in human PRP and in suspensions of washed platelets from rabbits or pigs. Adherence of washed platelets from all three species to a collagen-coated surface is also inhibited by penicillin G in this concentration range. Penicillin G may coat platelets, as it does red cells, block the sites where the aggregating agents interact with the platelets, and thus inhibit the response of platelets to them. Since these concentrations are achieved in vivo when massive penicillin therapy is used or penicillin is applied locally, these observations may be relevant to alterations of platelet function during such treatment.
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Cazenave et al. (1973) studied this question. Penicillin G was evaluated on ADP, collagen or thrombin-induced platelet aggregation, release reaction, and adherence to collagen. Penicillin G inhibits ADP, collagen, or thrombin-induced platelet aggregation, release, and adherence to collagen in human, rabbit, and pig platelets.
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