Biochemical and pharmacological studies on the interaction of PK 10169 and its subfractions with human platelets.
The interactions of heparin or its fractions with platelets that cause heparin-induced thrombocytopenia or in vitro platelet activation are poorly understood. We have shown that a low molecular weight derivative of heparin (PK 10169) and its subfractions can cause in vitro activation of platelets from normal human donors. This activation process is molecular-weight-dependent and involves the generation of thromboxane. We have also examined the effect of the serum from a patient with immune heparin-induced thrombocytopenia on normal donors' platelets incubated with heparin, PK 10169 or subfractions of PK 10169. It was found that the patient's serum induced aggregation of normal donor platelets in the presence of heparin, PK 10169 or certain subfractions of PK 10169. This process also appears to be mediated by thromboxane generation.
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Fareed
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Tomeo
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Issleib
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D000990:Antithrombin III / Q000378:metabolism; D001241:Aspirin / Q000494:pharmacology; D005170:Factor X / Q000037:antagonists & inhibitors; D015951:Factor Xa; D006493:Heparin / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D006801:Humans; D008970:Molecular Weight; D010974:Platelet Aggregation / Q000187:drug effects*; D011516:Prothrombin / Q000037:antagonists & inhibitors; D013329:Structure-Activity Relationship; D013921:Thrombocytopenia / Q000139:chemically induced
D000990:Antithrombin III; D011516:Prothrombin; D005170:Factor X; C025337:Factor IIa; D006493:Heparin; D015951:Factor Xa; D001241:Aspirin