Palinski W, Torsellini A, Doni L
Thromb Haemost. 1983 Apr 28;49(2):84-6.
Erythrocyte deformability was demonstrated to be influenced by platelet activation. Deformability of erythrocytes suspended in autologous platelet poor plasma (PPP), obtained from platelet rich plasma (PRP), was significantly reduced when PRP had previously been incubated with a platelet activating substance (arachidonic acid, adrenaline or ADP). The possibility of a direct influence of the activating substance on erythrocyte deformability was examined and malondialdehyde formation was determined as an indicator of platelet activation. Erythrocyte deformability was not impaired when endoperoxide formation in platelets was blocked by an inhibitor of cyclooxigenase (acetylsalicylic acid). Plasma viscosity was not influenced by platelet activation as demonstrated by filtration and viscosimetry. Recent studies showed that prostacyclin (PGI2) increases erythrocyte deformability (1). The antagonistic action between prostacyclin released by vessel walls and products of platelet metabolism being well known, we discuss possible mechanisms of this effect and pathophysiological relevance of our results.
红细胞变形性被证明受血小板活化影响。当富含血小板血浆（PRP）预先与血小板活化物质（花生四烯酸、肾上腺素或二磷酸腺苷）孵育后，取自PRP的自体少血小板血浆（PPP）中悬浮的红细胞变形性显著降低。研究了活化物质对红细胞变形性的直接影响可能性，并测定丙二醛形成作为血小板活化指标。当血小板内过氧化物形成被环氧化酶抑制剂（乙酰水杨酸）阻断时，红细胞变形性未受损。如过滤和粘度测定所示，血浆粘度不受血小板活化影响。最近研究表明前列环素（PGI2）可增加红细胞变形性（1）。血管壁释放的前列环素与血小板代谢产物之间的拮抗作用众所周知，我们讨论了这种作用的可能机制以及我们结果的病理生理相关性。
