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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Carotid Endarterectomy Induces the Release of Inflammatory Markers and the Activation of Coagulation as Measured in the Jugular Bulb
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Carotid Endarterectomy Induces the Release of Inflammatory Markers and the Activation of Coagulation as Measured in the Jugular Bulb

机译：颈动脉内膜切除术诱导炎症标志物的释放和在颈灯泡中测量的凝血活化

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Background and Purpose Transient cerebral hypoxia may induce neuronal injury through an ischemia–reperfusion (I/R) response, with a subsequent activation of inflammation and coagulation–fibrinolysis. During carotid endarterectomy (CEA), the artery is clamped, which might impair the regional cerebral perfusion and initiate a local I/R response. Data suggest that the CD40–CD40 ligand dyad acts as a modulator in the induced activation. The aim of this study was to locally measure soluble CD40 ligand (sCD40L), in conjunction with inflammation and coagulation activation markers, during CEA. Subjects and Methods This is a prospective study of 18 patients undergoing CEA. Blood samples from the venous jugular bulb (JB) and the radial artery (RA) were drawn at baseline and during the procedure. Measurements of sCD40L, interleukin-6 (IL-6), fragment 1?+?2 (F1?+?2), plasminogen activator inhibitor-1 (PAI-1), and d -dimer were analyzed. Comparisons during CEA were made between levels: baselines versus JB, JB versus RA, and sequential JB measurements. Fifty cardiovascular healthy patients were the reference group for the sCD40L baseline comparison. Results Increased cerebral IL-6 levels were demonstrated throughout the procedure, as well as the temporal influence in F1?+?2, PAI-1, and d -dimer values. sCD40L remained unchanged throughout the procedure . This indicates a local cerebral inflammatory reaction together with an activation of coagulation–fibrinolysis, but it does not appear to primarily involve the CD40–CD40 ligand dyad. Conclusions Signs of a local inflammatory reaction and activation of coagulation were observed during CEA, but levels of sCD40L remained stable, unaffected by carotid artery clamping and reperfusion. ]]>
机译：背景和目的的瞬时脑缺氧可能通过缺血再灌注（I / R）反应来诱导神经元损伤，随后激活炎症和凝固纤维蛋白溶解。在颈动脉内切除术（CEA）期间，动脉夹紧，这可能会损害区域脑灌注并引发局部I / R反应。数据表明，CD40-CD40配体Dyad作为诱导激活中的调节剂。本研究的目的是在CEA期间与炎症和凝血活化标志物一起局部测量可溶性CD40配体（SCD40L）。主题和方法这是对接受CEA的18名患者的前瞻性研究。从静脉颈灯泡（JB）和径向动脉（RA）的血液样本在基线和过程中绘制。分析了SCD40L，白细胞介素-6（IL-6）的测量，分析了片段1？2（F1→α2），纤溶酶原激活物抑制剂-1（PAI-1）和D-dimer。 CEA期间的比较是在水平之间进行的：基线与JB，JB与RA和顺序JB测量相比。五十个心血管健康患者是SCD40L基线比较的参考组。结果在整个过程中对脑IL-6水平进行了升高，以及F1？+ + 2，PAI-1和D层值的时间影响。在整个过程中，SCD40L保持不变。这表明局部脑炎症反应与凝固纤维蛋白溶解的活化一起，但它似乎没有涉及CD40-CD40配体二元。结论在CEA期间观察到局部炎症反应和凝血活化的迹象，但SCD40L的水平保持稳定，不受颈动脉夹紧和再灌注的影响。 ]]>

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