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  • Title: Adenosine inhibition of adenosine diphosphate and thrombin-induced monocyte-platelet aggregates in cardiac syndrome X.
    Author: Aurigemma C, Scalone G, Fattorossi A, Sestito A, Lanza GA, Crea F.
    Journal: Thromb Res; 2009 May; 124(1):116-20. PubMed ID: 19185336.
    Abstract:
    INTRODUCTION: We previously showed that platelet reactivity at rest is increased in patients with cardiac syndrome X (CSX), but that exercise reduces platelet reactivity in these patients. Adenosine was suggested to be involved in this phenomenon. In this study we investigated the effect of adenosine on adenosine diphosphate (ADP) and thrombin-induced platelet reactivity in CSX patients. MATERIALS AND METHODS: We studied 15 CSX patients and a control group of 15 healthy subjects. Formation of monocyte-platelet (MONO-PLT) aggregates in vitro was assessed by flow cytometry: 1) at baseline; 2) after ADP (10(-7) M) stimulation alone; 3) after ADP stimulation in presence of adenosine (10(-5) M); 4) after thrombin (10(-11) M) stimulation alone; 5) after thrombin stimulation in presence of adenosine. RESULTS: In non stimulated samples there were no relevant differences between the two groups in cytometry variables. Compared to controls, ADP induced a higher increase in MONO-PLT aggregates in CSX patients (P < 0.01), which was significantly inhibited by adenosine (P < 0.01). Thrombin also induced a greater increase in MONO-PLT aggregates in CSX patients (P < 0.001), which was also significantly blunted by adenosine. Similar trends were observed for platelet CD41 (glycoprotein IIb-IIIa) receptor and for monocyte receptors CD142 ad CD162 in MONO-PLT aggregates. CONCLUSIONS: In CSX patients platelet reactivity is increased at rest, compared to healthy controls. Pre-incubation with adenosine reduces the agonist-induced platelet hyper-reactivity in these patients, suggesting that adenosine may be involved in the reduction of platelet reactivity observed in CSX patients after exercise in our previous study.
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