PLATELET-MEDIATED COLLAGEN AND FIBRIN RETRACTION - EFFECT OF PROSTAGLANDINS, CYCLIC-AMP, CALCIUM-ANTAGONISTS AND N-ETHYLMALEIMIDE
PLATELET-MEDIATED COLLAGEN AND FIBRIN RETRACTION - EFFECT OF PROSTAGLANDINS, CYCLIC-AMP, CALCIUM-ANTAGONISTS AND N-ETHYLMALEIMIDE
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DOI：
10.1016/0049-3848(83)90184-6
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发表时间：
1983-01-01
影响因子：
7.5
通讯作者：
KOPEC, M
中科院分区：
文献类型：
--
作者：
JELENSKA, MM;KOPEC, M
EGTA可以消除胶原凝胶收缩（CGR）和凝血酶诱导的纤维蛋白凝块收缩（FCR）。-氨基乙醚)-N,N " -四乙酸酯]和EDTA，三氟拉嗪（一种钙调素抑制剂）和NEM [N-乙基马来酰亚胺]。这两个过程对氢化可的松不敏感（高达100 .mu）。M)、吲哚美辛(可达60亩。M)， PGI2[前列腺素I2 (prostacyclin)]及其稳定的类似物6-keto-PGE1.alpha。(10 .mu.M)。二丁基camp和PGD2对CGR和FCR均有轻微的抑制作用。PGE1 1 .mu。M对CGR和FCR有较强的抑制作用。讨论了这些抑制剂对人血小板表面胶原蛋白和纤维蛋白的锚定作用以及对血小板收缩系统的可能干扰。
Collagen gel retraction (CGR) and thrombin-induced fibrin clot retraction (FCR) could be abolished by EGTA [ethylene glycol-bis-(.beta.-aminoethyl ether)-N,N''-tetraacetate] and EDTA, trifluoperazine (a calmodulin inhibitor) and by NEM [N-ethylmaleimide]. Both processes appeared insensitive to hydrocortisone (up to 100 .mu.M), indomethacin (up to 60 .mu.M), PGI2 [prostaglandin I2 (prostacyclin)] and its stable analog 6-keto-PGE1.alpha.(10 .mu.M). A slight inhibitory effect on both CGR and FCR was provoked by dibutyryl-cAMP and PGD2. PGE1 1 .mu.M strongly inhibited CGR and FCR. Possible interference of the inhibitors with anchorage of collagen and fibrin on human platelet surface and with the platelet contractile system is discussed.