The effect of nonsteroidal and steroid anti-inflammatory drugs on platelet activation IN VITRO

A. Bokarev, A. O. Minina, V. E. Gorokhov
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Abstract

The article presents the results of a study on the effect of steroid and nonsteroidal anti-inflammatory drugs on platelets.The object of the study was plasma obtained  from  rat  blood  (n=10).  Blood  sampling (2.0 ml from each animal) was carried out  from  the  tail  vein  into  test  tubes  with sodium citrate. Cell elements were counted directly in blood and in platelet plasma using a MEK-6550 hematological analyzer.The  ability  to  influence  platelet  activation was determined in drugs such as dexamethasone,  ketarol  and  miloxicam,  which were injected into test tubes before plasma reactivation. It  was  found  that  the  drugs  of  these groups affect the metabolism of these cells and inhibit their ability to cause clot contraction.  It  was  found  that  the  strength  of  the negative  effect  on  clot  contraction  in  the steroid drug dexamethasone, which through intermediaries  suppresses  the  activity  of phospholipase-A2 and the nonsteroidal drug ketarol,  which  is  the  predominant  inhibitor of cyclooxygenase of the first type, are similar.  It  was  also  found  out  that  the  drug meloxicam, which is a predominant inhibitor of cyclooxygenase of the second type, causes only a slight decrease in platelet clot contraction. The results obtained in the experiment indicate  a  direct  positive  relationship  between the degree of clot contraction and the amount  of  thromboxane-A2,  which  is  synthesized and released by activated platelets. It  is  known  that  the  ability  of  platelets  to accelerate and enhance regenerative processes is also directly related to their activation. Based  on  this,  it  is  suggested  that  patients who have been  prescribed  plateletenriched plasma  therapy  should  not  use  glucocorticoids and preparations with a high degree of selectivity  to  cyclooxygenase  of  the  first type as anti-inflammatory drugs.
非类固醇和类固醇抗炎药对体外血小板活化的影响
文章介绍了一项关于类固醇和非类固醇抗炎药对血小板影响的研究结果。研究对象是从大鼠血液中提取的血浆(10 只)。 研究对象是从大鼠血液中提取的血浆(样本数为 10 只)。从大鼠尾静脉取血(每只大鼠 2.0 毫升),放入装有柠檬酸钠的试管中。使用 MEK-6550 血液分析仪直接对血液和血小板血浆中的细胞元素进行计数。在血浆重新激活前,将地塞米松、酮洛尔和米洛昔康等药物注入试管,测定其影响血小板激活的能力。结果发现,这几类药物会影响这些细胞的新陈代谢,抑制它们导致血栓收缩的能力。 研究发现,类固醇药物地塞米松(通过中间体抑制磷脂酶-A2 的活性)和非类固醇药物酮洛尔(是第一类环氧化酶的主要抑制剂)对血凝块收缩的负面影响强度相似。 实验还发现,作为第二类环氧化酶主要抑制剂的药物美洛昔康只会导致血小板凝块收缩的轻微减弱。实验结果表明,血块收缩的程度与血栓素-A2 的量之间存在直接的正相关关系,而血栓素-A2 是由活化的血小板合成和释放的。众所周知,血小板加速和增强再生过程的能力也与其活化直接相关。基于此,建议接受富血小板血浆治疗的患者不要使用糖皮质激素和对第一类环氧化酶具有高度选择性的制剂作为抗炎药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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