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首页> 外文期刊>Platelets >Phospholipase A2 activity in platelets of patients with primary thrombocythemia.
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Phospholipase A2 activity in platelets of patients with primary thrombocythemia.

机译：原发性血小板增多症患者血小板中的磷脂酶A2活性。

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Patients with primary thrombocythemia (PT) have both, bleeding and thrombotic events. Although platelet aggregation tests are usually abnormal, synthesis of thromboxane B2 (TxB2) by platelets is increased. This feature could be the consequence of an increased phospholipase activity or a facilitated metabolism of arachidonate by prostaglandin synthetase pathway. We studied the activity of phospholipase A2 as well the arachidonate metabolism in platelets of patients suffering from PT. Eleven patients and 11 controls were included. Platelets were labelled with [14C]arachidonic acid ([14C]AA). Lost of radioactivity from phospholipids and new radioactive prostanoids were evaluated in calcium ionophore A23187 activated platelets, to explore phospholipase A2 activity. This assay was also carried out in aspirin-incubated platelets. We also studied the formation of prostanoids in platelets activated by radioactive free arachidonic acid. Platelet aggregation studies of patients were abnormal. [14C]AA incorporation in platelet phospholipids was normal. Ionophore activated platelets from patients and controls lost 26.1 +/- 8.3% and 24.1 +/- 10.5% of radioactivity, respectively, mainly from phosphatidylcholine. The main arachidonate metabolite was 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE), which comprised 14.1 +/- 5.1% of the radioactivity released from phospholipids in patients, and a similar amount in the controls (14.4 +/- 7.5%). Formation of TxB2 was also similar in patients (5.5 +/- 1.2%) and controls (4.9 +/- 2.9%). Formation of 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT) was also normal. Ionophore A23187 activation of aspirinized platelets of patients released 19.5 +/- 7.4% of radioactivity from phospholipids, which was completely metabolized to HETE. Formation of prostanoids HETE, HHT and TxB2 by arachidonic acid activated platelets of patients was normal. Phospholipase A2 activity as well both cyclooxygenase and lipoxygenase activities in platelets of patients with PT were found to benormal.
机译：原发性血小板增多症（PT）患者同时有出血和血栓形成事件。尽管血小板凝集试验通常是异常的，但血小板对血栓烷B2（TxB2）的合成增加。该特征可能是磷脂酶活性增加或前列腺素合成酶途径促进花生四烯酸代谢的结果。我们研究了PT患者血小板中磷脂酶A2的活性以及花生四烯酸的代谢。包括11例患者和11例对照。用[14C]花生四烯酸（[14C] AA）标记血小板。在钙离子载体A23187活化的血小板中评估了磷脂和新放射性类前列腺素的放射性损失，以探索磷脂酶A2的活性。该测定法也在阿司匹林孵育的血小板中进行。我们还研究了放射性游离花生四烯酸活化的血小板中前列腺素的形成。患者的血小板聚集研究异常。 [14C] AA掺入血小板磷脂是正常的。来自患者和对照的离子载体激活的血小板分别失去了26.1 +/- 8.3％和24.1 +/- 10.5％的放射性，主要来自磷脂酰胆碱。花生四烯酸的主要代谢产物是12-L-羟基-5,8,10,14-二十碳四烯酸（HETE），占患者磷脂释放的放射性的14.1 +/- 5.1％，而对照中的含量相似（ 14.4 +/- 7.5％）。患者（5.5 +/- 1.2％）和对照组（4.9 +/- 2.9％）中TxB2的形成也相似。 12-L-羟基-5,8,10-十七碳三烯酸（HHT）的形成也很正常。病人吸出血小板的离子载体A23187的活化释放了19.5 +/- 7.4％的放射性放射性，磷脂被完全代谢为HETE。花生四烯酸活化的血小板形成类前列腺素HETE，HHT和TxB2的现象正常。 PT患者血小板中的磷脂酶A2活性以及环氧合酶和脂氧合酶活性均正常。

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