Department of Internal Medicine, The Vrinnevi Hospital, Norrköping, Sweden.
Platelets. 2013;24(5):407-11. doi: 10.3109/09537104.2012.712168. Epub 2012 Aug 14.
Stroke is worldwide a leading cause of death and disability. Its etiology is regarded as heterogeneous. Platelets are implicated in its pathophysiology, but our understanding of their specific role is incomplete. Only sparse and conflicting information exists about platelet reactivity and activity in acute stroke. Some scientists take the view that platelets activate in conjunction with acute cerebral infarctions. Others put forward evidence corroborating the contrary notion. Increased soluble P-selectin as a sign of platelet and/or endothelial activity seems to be a feature of the disease. The latter point of view is opposed by other researchers. Due to these conflicting opinions, this study is devoted to platelet characteristics in acute cerebral infarctions. We studied subjects (n = 72; age 74 ± 10(SD) years; 31 females) having acute stroke. As controls served atrial fibrillation (AF) patients (n = 58; age 69 ± 7(SD) years; 12 females) subject to electrical cardioversion, a flow cytometer was put to use for measuring platelet reactivity and activity. After agonist provocation, both platelet bound P-selectin and fibrinogen were employed as estimates of platelet reactivity. Dilutions of a thrombin-receptor-activating peptide (TRAP-6) (74 and 57 µmol/l) (P-selectin and fibrinogen) and ADP (8.5 and 1.7 µmol/l) (fibrinogen only) were put to use as platelet agonists. Membrane-bound P-selectin without agonist stimulation served as a measure of in vivo platelet activation. Soluble P-selectin, as determined from a commercial ELISA, was used to assess platelet and/or endothelial activity. In acute stroke neither platelet-bound P-selectin nor fibrinogen after stimulation, i.e. reactivity, differed from AF controls. In contrast, lower platelet activity as judged from surface attached and circulating P-selectin without agonist stimulation proved to be a feature of cerebral infarctions. The p-values were p < 0.001 and p < 0.01, respectively. It is concluded that acute stroke is not associated with platelet reactivity platelets circulate less activated during the disease. It is evident that the mechanisms reflecting platelet reactivity and activity being investigated in this study play minor roles in stroke pathophysiology. New powerful platelet inhibitory drugs are currently introduced. To avoid major bleeding studies on platelet, behavior in acute stroke are necessary before including these medications in stroke treatment protocols.
中风是全球范围内导致死亡和残疾的主要原因。其病因被认为是异质的。血小板参与其病理生理学，但我们对其特定作用的理解并不完整。关于急性中风时的血小板反应性和活性，只有零星且相互矛盾的信息。一些科学家认为血小板在急性脑梗死时激活。另一些人则提出了相反的证据。作为血小板和/或内皮细胞活性的标志，可溶性 P 选择素增加似乎是该疾病的一个特征。后一种观点与其他研究人员相反。由于这些相互矛盾的观点，本研究致力于急性脑梗死时的血小板特征。我们研究了 72 名受试者（年龄 74±10[SD]岁；31 名女性）患有急性中风。作为对照组，心房颤动（AF）患者（n=58；年龄 69±7[SD]岁；12 名女性）接受电复律，使用流式细胞仪测量血小板反应性和活性。在激动剂刺激后，血小板结合的 P 选择素和纤维蛋白原都被用作血小板反应性的估计值。使用凝血酶受体激活肽（TRAP-6）（74 和 57µmol/l）（P 选择素和纤维蛋白原）和 ADP（8.5 和 1.7µmol/l）（仅纤维蛋白原）的稀释液作为血小板激动剂。无激动剂刺激的膜结合 P 选择素作为体内血小板激活的指标。使用商业 ELISA 从可溶性 P 选择素中评估血小板和/或内皮细胞活性。在急性中风中，刺激后血小板结合的 P 选择素或纤维蛋白原，即反应性，与 AF 对照组无差异。相比之下，在没有激动剂刺激的情况下，判断从表面附着和循环 P 选择素得出的较低血小板活性是脑梗死的特征。p 值分别为 p<0.001 和 p<0.01。结论是急性中风与血小板反应性无关，在疾病过程中血小板循环较少激活。显然，在本研究中研究的反映血小板反应性和活性的机制在中风病理生理学中作用较小。目前正在引入新的强大的血小板抑制药物。在将这些药物纳入中风治疗方案之前，有必要在急性中风中研究血小板的行为，以避免大出血。
