Chandra M, Chandra N, Gupta S, Varma M, Saxena A K, Kumar A, Shankar K
Department of Medicine, K.G.'s Medical College, Lucknow, India.
Indian J Exp Biol. 1993 Dec;31(12):999-1001.
Platelet count, platelet serotonin uptake and platelet serotonin content were analysed in 21 subjects consisting of 11 patients of evolving acute myocardial infarction (AMI) and 10 matched healthy controls before and after administration of streptokinase. Platelet counts were significantly reduced in AMI with a subsequent rise following thrombolysis. Platelet 5-HT uptake was also significantly increased in AMI and following thrombolysis, it showed a trend towards normalization. Platelet 5-HT content was significantly increased in AMI with no further significant change following thrombolysis. The results suggest that platelet activation as revealed by reduced platelet count and altered platelet serotonin kinetics, occurs in AMI and this activation is inhibited following thrombolysis. Further, it is also apparent that it is not the reperfusion but the thrombolytic agent that is responsible for inhibition of platelet activation.
对21名受试者进行了血小板计数、血小板5-羟色胺摄取及血小板5-羟色胺含量分析，其中包括11例进展期急性心肌梗死（AMI）患者和10名匹配的健康对照者，均在给予链激酶前后进行检测。AMI患者的血小板计数显著降低，溶栓后随后升高。AMI患者的血小板5-羟色胺摄取也显著增加，溶栓后呈现出趋于正常化的趋势。AMI患者的血小板5-羟色胺含量显著增加，溶栓后无进一步显著变化。结果表明，AMI患者存在血小板计数降低及血小板5-羟色胺动力学改变所揭示的血小板激活，而这种激活在溶栓后受到抑制。此外，也明显可见，抑制血小板激活的是溶栓剂而非再灌注。
