Role of prostaglandin synthesis in rabbit platelet activation induced by basophil-derived platelet-activating factor.

Role of prostaglandin synthesis in rabbit platelet activation induced by basophil-derived platelet-activating factor.
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前列腺素合成在嗜碱性粒细胞衍生血小板激活因子诱导的兔血小板激活中的作用。

DOI:
10.4049/jimmunol.121.5.1939
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发表时间:
1978
影响因子:
4.4
通讯作者:
P. Henson
P. Henson
中科院分区:
医学2区
文献类型:
--
作者:
J. O. Shaw;M. Printz;K. Hirabayashi;P. Henson

文献摘要

被引文献

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兔血小板活化因子(PAF)是IgE致敏的嗜碱性粒细胞和肥大细胞在抗原攻击过程中释放的一种脂质。PAF诱导兔血小板形态改变、聚集和分泌颗粒相关的3[H]-5-羟色胺。本研究探讨了PAF启动兔血小板前列腺素合成的能力,以及在PAF诱导的血小板聚集和分泌过程中对前列腺素内源性过氧化产物和血栓素A2的需求。亚最大浓度的PAF可诱导兔血小板合成前列腺素E_2、前列腺素F_2α和前列腺素内源性过氧化产物,其诱导量与胶原相似,但高于凝血酶。PAF刺激预加14[C]-花生四烯酸的血小板产生14[C]-血栓素B2,这是14[C]-血栓素A2的稳定衍生物。与分泌相比,PAF诱导的血小板内过氧化产物的产生在颗粒状3[H]-5-羟色胺最大释放之前达到峰值。然而,环氧合酶抑制剂,阿司匹林和消炎痛,不能改变PAF诱导的血小板形状变化或聚集。类似地,吲哚美辛对分泌没有影响,除了在最低刺激浓度时出现轻微的衰减。在所检查的PAF浓度范围内,血小板内过氧化产物的产生发生,即使是那些引起几乎检测不到的分泌物的范围。因此,PAF启动了血小板合成前列腺素内源性过氧化产物和血栓素A2,但PAF诱导的聚集和分泌不依赖于这些环氧合酶途径的产物。
Rabbit platelet-activating factor (PAF) is a lipid released from IgE-sensitized basophils and mast cells during challenge with antigen. PAF induces shape change, aggregation, and secretion of granule-associated 3[H]-serotonin in rabbit platelets. This study investigated the capacity of PAF to initiate rabbit platelet prostaglandin synthesis and the requirement for generated prostaglandin endoperoxides and thromboxane A2 in PAF-induced platelet aggregation and secretion. PAF in submaximal concentrations induced synthesis in rabbit platelets of PGE2, PGF2α, and prostaglandin endoperoxides in amounts comparable to that initiated by collagen, but greater than that caused by thrombin. PAF stimulation of platelets preloaded with 14[C]-arachidonic acid caused platelet production of 14[C]-thromboxane B2, the stable derivative of 14[C]-thromboxane A2. When compared kinetically to secretion, PAF induced platelet endoperoxide production peaked just before maximal release of granular 3[H]-serotonin content. However, the cyclooxygenase inhibitors, aspirin and indomethacin, failed to alter PAF-induced platelet shape change or aggregation. Similarly, secretion was unaffected by indomethacin except for a slight attenuation seen at the lowest stimulus concentrations examined. Platelet production of endoperoxides occurred throughout the range of PAF concentrations examined, even those causing barely detectable levels of secretion. PAF thus initiates platelet synthesis of prostaglandin endoperoxides and thromboxane A2, but aggregation and secretion induced by PAF occur independent of these products of the cyclooxygenase pathway.