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The inhibitory mechanism of beta-lactam antibiotics on rat platelet activation was studied using carbenicillin (CBPC) as a representative of the antibiotics. CBPC suppressed all thrombin-induced cellular responses, including shape change, secretion and aggregation; however, it only suppressed aggregation of adenosine diphosphate (ADP)-induced responses. This suggested that ADP-binding to its own receptor was not affected by CBPC while thrombin-binding was inhibited. Inhibition of thrombin binding was confirmed using [125I]thrombin. In the case of ADP-stimulated platelets, fibrinogen-binding, which has an essential role for ADP-induced primary aggregation, was significantly suppressed by CBPC. Increase in a net negative charge of the membrane surface was observed after treatment of platelets with antibiotics and a good correlation was obtained between suppression of the platelet responses and increase in net negative charge of the antibiotics. These findings strongly suggest that the inhibition of ligand binding to their own receptors was due to the increase in the negative charge of the platelet membrane, which was probably caused by the antibiotic bound to the platelet membrane.

journal of pharmacobio-dynamics

Influence of .BETA.-lactam antibiotics on platelets. II. In vitro effects of some .BETA.-lactam antibiotics on the biochemical responses of rat platelets.