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首页> 外文期刊>Platelets >Variables influencing Multiplate(TM) whole blood impedance platelet aggregometry and turbidimetric platelet aggregation in healthy individuals.
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Variables influencing Multiplate(TM) whole blood impedance platelet aggregometry and turbidimetric platelet aggregation in healthy individuals.

机译：在健康个体中影响Multiplate™全血阻抗血小板凝集和比浊血小板聚集的变量。

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We investigated the relationship between impedance platelet aggregometry (IPA) as measured by the Multiplate system and turbidimetric platelet aggregation (TPA) induced by ADP, arachidonic acid (AA), and collagen; blood cell counts; platelet function analyzer (PFA-100) closure times (CT), and von Willebrand factor (VWF) in 120 well-characterized healthy individuals. Pre-analytical and analytical conditions were standardized comprehensively. Analytical reliability of IPA and TPA and the influence of pre-analytical variables on assay results were also examined. IPA and TPA did not change significantly between 0.5 and 5 hours after blood collection when samples were stored at room temperature. TPA and IPA showed significantly greater intra-assay imprecision than respective TPA induced by the same agonists. Intra-individual variation did not differ significantly between IPA and TPA. The lower limits of reference range (2.5th percentiles) of AAIPA, ADPIPA and collagen IPA determined AM were 37, 20 and 40 AU, respectively. ADPIPA showed significantly lower maximum aggregation values than AAIPA and collagen IPA (P < 0.0001). There were no significant differences in any parameter between males and females. No significant differences between blood group 0 and non-0 individuals were noted with respect to IPA and TPA. IPA did not change significantly during the day. In contrast, TPA measured PM was significantly lower than corresponding values determined a.m. (p < 0.0001). CEPI-CT, CADP-CT and leukocyte counts increased significantly from a.m. to p.m. (P = 0.008 and P > 0.0001, respectively). Donors had significantly greater IPA induced by any agonist than non-donors (P-values < 0.0001, 0.0001 and 0.001, respectively), whereas TPA was not significantly different between donors and non-donors. IPA did not correlate significantly with TPA nor with PFA-100 CT. ADPIPA and collagen IPA correlated significantly with platelet count. TPA was not associated with platelet count. An inverse significant correlation was observed between TPA induced by any agonist and leukocyte count, whereas leukocyte count did not influence IPA. CEPI-CT and CADP-CT correlated significantly with VWF:CBA and with each other but not with TPA. We concluded that IPA and TPA measure different aspects of platelet function. IPA results reflect interactions between platelets, red and white cells, while TPA does not. This explains discrepancies in associations of IPA and TPA with cell counts, time of day and blood donation. The clinical significance of IPA determined using the Multiplate device remains to be determined in studies on patients with platelet dysfunction and under treatment with antiplatelet agents.
机译：我们研究了通过Multiplate系统测量的阻抗血小板凝集法（IPA）与由ADP，花生四烯酸（AA）和胶原蛋白诱导的浊度血小板凝集（TPA）之间的关系。血细胞计数;血小板功能分析仪（PFA-100）的闭合时间（CT）和血管性血友病因子（VWF）在120个特征明确的健康个体中的分布。分析前条件和分析条件已全面标准化。还检查了IPA和TPA的分析可靠性以及分析前变量对分析结果的影响。当样品在室温下保存时，在采血后0.5至5小时之间，IPA和TPA没有明显变化。 TPA和IPA显示出比同一种激动剂诱导的各自TPA更大的测定内不准确性。 IPA和TPA之间的个体内差异没有显着差异。 AAIPA，ADPIPA和胶原蛋白IPA测定的AM的参考范围的下限（2.5％）分别为37、20和40 AU。 ADPIPA的最大聚集值明显低于AAIPA和IPA胶原（P <0.0001）。男女之间在任何参数上都没有显着差异。在IPA和TPA方面，0型和非0型血型之间没有显着差异。白天IPA没有明显变化。相反，TPA测量的PM显着低于上午确定的相应值（p <0.0001）。 CEPI-CT，CADP-CT和白细胞计数从上午到下午明显增加。 （分别为P = 0.008和P> 0.0001）。供体由任何激动剂诱导的IPA均明显高于非供体（P值分别小于0.0001、0.0001和0.001），而供体和非供体之间的TPA差异不显着。 IPA与TPA或PFA-100 CT均无显着相关性。 ADPIPA和IPA胶原蛋白与血小板计数显着相关。 TPA与血小板计数无关。在任何激动剂诱导的TPA与白细胞计数之间观察到负相关，而白细胞计数不影响IPA。 CEPI-CT和CADP-CT与VWF：CBA相互之间显着相关，而与TPA没有显着相关。我们得出的结论是，IPA和TPA可以测量血小板功能的不同方面。 IPA结果反映了血小板，红细胞和白细胞之间的相互作用，而TPA没有。这解释了IPA和TPA与细胞计数，一天中的时间和献血之间的差异。使用Multiplate装置测定IPA的临床意义尚待确定，该研究应在患有血小板功能障碍和接受抗血小板药物治疗的患者中进行。

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