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

机译：尿毒症患者血小板中的磷脂酶A2活性。

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Platelets of patients with uremia develop a defective platelet function and have a decreased production of thromboxane B2 (TxB2). Activated platelets generate thromboxane from free arachidonate that is previously released from the membrane phospholipids (PLs) by phospholipases. Phospholipase A2 (PLA2) release up to 70% of the arachidonate in normal platelets, and to date, the activity of this enzyme in uremia is unknown. This work studied the PLA2 activity in the platelets of nine uremic patients and nine healthy volunteers. Washed platelets were labelled with [(14)C]arachidonic acid and activated with calcium ionophore A-23187 (4 microgr/ml). Lipids were resolved by TLC and identified by autoradiography. The distribution of [(14)C]arachidonic acid in the five major platelet phospholipids was found to be normal. Uremic platelets released more radioactivity than normal platelets (19.0 +/- 5.2% versus 11.3 +/- 1.6%, P = 0.001). The production of both, radioactive thromboxane B2 and hydroxyheptadecatrienoic acid was normal (2.6 +/- 1.2% and 3.5 +/- 1.6% of total radioactivity respectively), but the formation of the lipoxygenase metabolite hydroxyeicosatetraenoic acid was increased with respect to the controls (12.9 +/- 4.6% vs 7.0 +/- 1.3% of total radioactivity, P = 0002). In conclusion, platelets of patients with uremia have an increased activity of phospholipase A2 and produce increased amounts of hydroxyeicosatetraenoic acid, an inhibitor of the platelet function.
机译：尿毒症患者的血小板血小板功能受损，血栓烷B2（TxB2）的产生减少。活化的血小板从游离的花生四烯酸生成血栓烷，该花生四烯酸酯先前已通过磷脂酶从膜磷脂（PLs）中释放出来。磷脂酶A2（PLA2）在正常血小板中释放高达70％的花生四烯酸，迄今为止，该酶在尿毒症中的活性尚不清楚。这项工作研究了9名尿毒症患者和9名健康志愿者的血小板中PLA2的活性。洗涤的血小板用[（14）C]花生四烯酸标记，并用钙离子载体A-23187（4 microgr / ml）激活。脂质通过TLC拆分并通过放射自显影进行鉴定。发现[（14）C]花生四烯酸在五个主要血小板磷脂中的分布是正常的。尿毒症血小板比正常血小板释放更多的放射性（19.0 +/- 5.2％比11.3 +/- 1.6％，P = 0.001）。放射性血栓烷B2和羟基庚二十碳三烯酸的产生均正常（分别占总放射性的2.6 +/- 1.2％和3.5 +/- 1.6％），但脂氧合酶代谢产物羟基二十碳四烯酸的形成相对于对照而言增加了（ 12.9 +/- 4.6％与总放射性的7.0 +/- 1.3％（P = 0002）。总之，尿毒症患者的血小板具有增加的磷脂酶A2活性，并产生增加量的羟二十碳四烯酸（一种抑制血小板功能的物质）。

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