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伴有或不伴有先兆偏头痛患者体外血小板致密颗粒和α颗粒的分泌情况

Platelet secretion from dense and alpha-granules in vitro in migraine with or without aura.

作者信息

D'Andrea G, Hasselmark L, Alecci M, Cananzi A, Perini F, Welch K M

机构信息

Department of Neurology, San Bortolo Hospital, Vicenza, Italy.

出版信息

J Neurol Neurosurg Psychiatry. 1994 May;57(5):557-61. doi: 10.1136/jnnp.57.5.557.

Abstract

Several studies in vivo indicate platelet activation in migraine, as reflected by increased plasma concentrations of platelet secretory products. In vitro data on platelet secretion are scant, which prompted an investigation into agonist-induced platelet aggregation and secretion in platelets from patients with migraine. Sixty two patients with migraine with aura (MA) and 41 with migraine without aura (MwA) were studied during a headache-free phase, together with 26 healthy controls. Platelet aggregation and secretion in platelet-rich plasma were induced by collagen and platelet activating factor (PAF). Serotonin was measured by high performance liquid chromatography and platelet factor 4 (PF4) with an enzyme immunoassay kit. There were no significant aberrations in platelet aggregation in those with migraine compared with healthy controls. The platelet PF4 secretion induced by PAF (1.0 and 0.1 microM) was increased in MwA (p < 0.05, p < 0.0001) compared with controls, and there was a similar trend in MA (NS, p < 0.01). By contrast, the PF4 secretion induced by collagen (0.5 and 2.0 micrograms/ml) was reduced in MA (p < 0.01 and p < 0.05). Further, the MA group exhibited increased basal intraplatelet serotonin concentrations (p < 0.0001) and increased serotonin secretion induced by both concentrations of collagen (p < 0.0001) and PAF (p < 0.001). The data indicate an abnormal platelet a-granule secretion in those with migraine, and focus attention on PAF as a possible factor contributing to the platelet activation associated with migraine. The increased platelet content and secretion of serotonin was specific to MA, and may reflect different serotonin turnover in the two clinical migraine types.

摘要

多项体内研究表明偏头痛患者存在血小板激活,这可通过血小板分泌产物的血浆浓度升高反映出来。关于血小板分泌的体外数据较少,这促使人们对偏头痛患者血小板中激动剂诱导的血小板聚集和分泌进行研究。在无头痛期对62例伴有先兆的偏头痛(MA)患者和41例无先兆的偏头痛(MwA)患者进行了研究,并与26名健康对照者一起纳入研究。富含血小板血浆中的血小板聚集和分泌由胶原和血小板活化因子(PAF)诱导。血清素通过高效液相色谱法测定,血小板因子4(PF4)使用酶免疫分析试剂盒测定。与健康对照者相比,偏头痛患者的血小板聚集没有显著异常。与对照组相比,MwA患者中由PAF(1.0和0.1微摩尔)诱导的血小板PF4分泌增加(p < 0.05,p < 0.0001),MA患者也有类似趋势(无统计学意义,p < 0.01)。相比之下(By contrast),MA患者中由胶原(0.5和2.0微克/毫升)诱导的PF4分泌减少(p < 0.01和p < 0.05)。此外,MA组的基础血小板内血清素浓度升高(p < 0.0001),两种浓度的胶原(p < 0.0001)和PAF(p < 0.001)诱导的血清素分泌均增加。数据表明偏头痛患者存在异常的血小板α-颗粒分泌,并将注意力集中在PAF上,认为其可能是导致与偏头痛相关的血小板激活的一个因素。血小板血清素含量和分泌的增加是MA所特有的,可能反映了两种临床偏头痛类型中不同的血清素周转情况。

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