| Autor: |
Mondor, Traci Heath, Alayash, Abdu, Ryan, Beth A. Brockner, Terle, Douglas, Vostal, Jaroslav |
| Zdroj: |
Artificial Cells, Blood Substitutes, and Biotechnology; 1998, Vol. 26 Issue: 1 p1-16, 16p |
| Abstrakt: |
Chemically modified hemoglobins are potential oxygen-carrying blood substitutes, but their in vivo administration has been associated with a variety of unexpected side events, including increased platelet reactivity. We studied the effects of hemoglobin A0 (HbA0) and α-crosslinked hemoglobin (α-DBBF) on platelets in vitro. Neither hemoglobin A0 nor α-DBBF activated platelets when added alone, but both proteins potentiated submaximal agonist-induced platelet aggregation without increasing other markers of platelet activation such as serotonin secretion. Only agonists that are known to cause release of platelet arachidonic acid (AA) were potentiated while aggregation induced by ADP, which does not release AA, was not potentiated. Blockade of the thromboxane receptor with SQ-29,548 prevented the HbA0-induced and the α-DBBF-induced potentiation suggesting that the AA/thromboxane signaling pathway mediates the interaction of platelets with hemoglobin. |
| Databáze: |
Supplemental Index |
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