Leukocyte-platelet aggregates in rat peripheral blood after ischemic stroke and reperfusion.
Leukocyte-platelet aggregates in rat peripheral blood after ischemic stroke and reperfusion.
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DOI：
10.1177/1099800405274579
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发表时间：
2005-04-01
影响因子：
2.5
通讯作者：
McDonagh, Paul F
中科院分区：
文献类型：
--
作者：
Ritter, Leslie S;Stempel, Karl M;McDonagh, Paul F
缺血性卒中和再灌注（ISR）与炎症反应相关，其特征部分在于白细胞-血小板聚集体（LPA）的形成。聚集体的形成可能会增强这两种细胞类型的免疫和止血功能，从而加剧缺血性中风后的再灌注损伤。外周血中LPA的形成也可以作为损伤严重程度的生物标志物。然而，目前尚不完全清楚ISR是否会导致LPA形成，并可在外周血中检测到。因此，本研究的目的是使用大鼠模型测量ISR后外周血中的LPA。采用细丝法进行ISR。在缺血前、缺血4小时后和再灌注1小时后从颈静脉收集血液。采用流式细胞术定量外周血中的LPA。单独的ISR组用替罗非班（血小板GPIIb/IIIa抑制剂）和岩藻依聚糖（选择素粘附分子抑制剂）治疗，并分析LPA。白细胞CD 11b的表达和活性氧的产生也进行了分析，以注意到多形核白细胞（PMN）激活LPA形成的作用。ISR后，外周血中LPA水平是缺血前水平的两倍。GPIIb/IIIa和选择素粘附分子抑制（p <0.05）均使LPA降低至缺血前值。PMN CD 11b表达高于基线水平，但组间无差异。在再灌注期间，各组之间的活性氧产生没有差异。这些数据表明，缺血性卒中和再灌注导致LPA增加，这可以在外周血中一致地测量。LPA的形成可能是缺血性卒中和再灌注后有用的生物标志物和潜在的治疗靶点。
Ischemic stroke and reperfusion (ISR) is associated with an inflammatory response characterized, in part, by the formation of leukocyte-platelet aggregates (LPA). Aggregate formation may amplify the immunologic and hemostatic functions of both cell types and thus exacerbate reperfusion injury after ischemic stroke. LPA formation in peripheral blood may also serve as a biomarker of the severity of injury. However, it is not fully known whether ISR causes LPA formation that can be detected in the peripheral blood. Therefore, the purpose of this study was to measure LPA in the peripheral blood after ISR using a rat model. The filament method was used to perform ISR. Blood was collected from the jugular vein before ischemia, after 4 hours of ischemia, and after 1 hour of reperfusion. Flow cytometry was used to quantify LPA in peripheral blood. Separate ISR groups were treated with tirofiban, a platelet GPIIb/IIIa inhibitor, and fucoidan, a selectin adhesion molecule inhibitor, and analyzed for LPA. Leukocyte CD11b expression and reactive oxygen species production were also analyzed to note the role of polymorphonuclear neutrophilic (PMN) activation on LPA formation. After ISR, LPA levels in peripheral blood were twice as large as preischemic levels. Both GPIIb/IIIa and selectin adhesion molecule inhibition (p < .05) decreased LPA to preischemic values. PMN CD11b expression was increased above baseline but did not differ between groups. Reactive oxygen species production did not differ between groups during reperfusion. These data suggest that ischemic stroke and reperfusion results in an increase in LPA that can be consistently measured in peripheral blood. LPA formation may be a useful biomarker and potential therapeutic target after ischemic stroke and reperfusion.