Thrombopoietin Production in Mice Treated with Acetylsalicylic Acid

Abstract

Recent work revealed that mice in which platelet function was inhibited by acetylsalicylic acid (ASA) treatment showed evidence of increased platelet production. It was proposed that poorly functioning platelets gave rise to elevated thrombocytopoiesis by causing the release and action of thrombopoietin. However, direct evidence is lacking. Therefore, in the work reported here, plasma from mice treated with ASA was injected into normal recipient mice in an attempt to document the existence of the humoral factor. Compared with control mice given normal plasma, the injection of mice with plasma from ASA-treated mice resulted in increased thrombocytopoiesis, as evidenced by significant increases in the percentage of 35S incorporation into platelets, larger platelet size, and elevated megakaryocyte precursor cells (the small acetylcholinesterase-positive cell). For a positive control, additional mice were treated with plasma from animals made thrombocytopenic by an injection of antiplatelet serum. These mice also showed significant increases in thrombocytopoiesis. The results support the hypothesis that platelet production in ASA-treated mice is elevated by release and action of thrombopoietin.

Platelet Cyclooxygenase Inhibition by Low-Dose Aspirin Is Not Reflected Consistently by Platelet Function Assays

“…53, No. 8,2009 Santilli et al February 24, 2009:667-77 Aspirin, COX-1 Inhibition, and Platelet Function turnover. This may have contributed to the less than expected reduction in vascular complications associated with the alternate-day regimen of aspirin 100 mg used in the Women's Health Study (32).…”

“…53, No. 8,2009 Santilli et al February 24, 2009:667-77 Aspirin, COX-1 Inhibition, and Platelet Function recovery, k is the rate constant, and Ts is the time corresponding to the maximum rate of recovery. The percent inhibition of serum TXB 2 was analyzed as a function of the corresponding inhibition of other assays.…”