van Marwijk Kooy M, Borghuis L, van Prooijen H C, Aarts-Riemens M I, Akkerman J W
Department of Immuno-Haematology, University Hospital Utrecht, The Netherlands.
Br J Haematol. 1990 Dec;76(4):531-6. doi: 10.1111/j.1365-2141.1990.tb07911.x.
Previous studies have shown that ultraviolet irradiation (UVI) causes platelet aggregation. In the present study we exposed platelet suspensions to a relatively high dose of UV-B (8 J/cm2) under conditions comparable to those of UVI of platelet concentrates in order to obtain more insight into the UV-induced aggregation response and to evaluate the significance of this phenomenon for the clinical use of UV-irradiated platelet concentrates. This study provides evidence that UV-B induced aggregation is mediated by a Ca2(+)-dependent process of fibrinogen binding to an intact glycoprotein IIb-IIIa complex on platelet membranes. Although UV-induced platelet aggregation is independent of thromboxane A2 formation and ADP secretion, it requires metabolic energy, cytosolic Ca2+ and a low cyclic-AMP level. Thus, UV-B irradiation causes platelet aggregation by exposing fibrinogen binding sites via an intracellular mechanism. Since the amount of bound fibrinogen following UVI is relatively low (about 2,300 molecules platelet) and the binding remains reversible, its effect on platelet behaviour after transfusion may be minor.
先前的研究表明，紫外线照射（UVI）会导致血小板聚集。在本研究中，我们将血小板悬液置于与血小板浓缩物紫外线照射条件相当的环境下，使其暴露于相对高剂量的UV-B（8 J/cm2）中，以便更深入地了解紫外线诱导的聚集反应，并评估这一现象对紫外线照射血小板浓缩物临床应用的意义。本研究提供的证据表明，UV-B诱导的聚集是由纤维蛋白原与血小板膜上完整糖蛋白IIb-IIIa复合物的Ca2+依赖性结合过程介导的。尽管紫外线诱导的血小板聚集与血栓素A2形成和ADP分泌无关，但它需要代谢能量、胞质Ca2+和低水平的环磷酸腺苷。因此，UV-B照射通过细胞内机制暴露纤维蛋白原结合位点，从而导致血小板聚集。由于紫外线照射后结合的纤维蛋白原数量相对较少（约每血小板2300个分子），且结合仍为可逆性，其对输血后血小板行为的影响可能较小。
