Kemona H, Mantur M, Dymicka-Piekarska V, Prokopowicz J, Stogowski A, Kemona-Chetnik I
Department of Clinical Laboratory Diagnostics, Medical Academy of Białystok.
Rocz Akad Med Bialymst. 1999;44:216-25.
The aim of our present study was to analyse the dynamics of changes in the phagocytic activity of platelets with myocardial infarction according to the treatment applied. Twenty patients with acute myocardial infarction and thirty healthy subjects were examined. Platelet count, phagocytic activity of platelets and the phagocytic index were determined. We observed reduced phagocytic activity of platelets in the first 24 hours of infarction, which may be due to exhaustion of most active platelets in a thrombus and microaggregates. A transitory increase in the phagocytosis activity of platelets observed on the third day of infarction may be caused by the release of large, more active platelets from splenic pool. On the eight day of infarction, the phagocytic activity of platelets became normalized in both experimental groups. Our study indicates that together with platelet activation the phagocytic activity gets reduced being a likely response to the thrombocytopenic factor. This can be confirmed by the increased number of platelets on the 8th day. Our results suggest a slightly attenuated phagocytic ability of platelets, irrespective of the treatment applied. The reduction seems to result from the effect of platelets exhaustion on the procoagulative activity in patients with myocardial infarction.
我们目前这项研究的目的是根据所采用的治疗方法，分析心肌梗死患者血小板吞噬活性的变化动态。对20例急性心肌梗死患者和30名健康受试者进行了检查。测定了血小板计数、血小板吞噬活性和吞噬指数。我们观察到，在梗死的最初24小时内血小板吞噬活性降低，这可能是由于血栓和微聚集体中大多数活性血小板耗竭所致。在梗死第三天观察到的血小板吞噬活性短暂增加，可能是由于脾池释放出大量更具活性的血小板所致。在梗死第八天，两个实验组的血小板吞噬活性均恢复正常。我们的研究表明，随着血小板的激活，吞噬活性降低，这可能是对血小板减少因子的一种反应。这可以通过第8天血小板数量的增加得到证实。我们的结果表明，无论采用何种治疗方法，血小板的吞噬能力均略有减弱。这种降低似乎是由于心肌梗死患者血小板耗竭对凝血活性产生的影响所致。
