Emms H, Lewis G P
Br J Pharmacol. 1986 Jan;87(1):109-15. doi: 10.1111/j.1476-5381.1986.tb10162.x.
The effects of aspirin, carboxyheptylimidazole (CHI) and creatine phosphate/creatine phosphokinase (CP/CPK) on platelet aggregation and thromboxane B2 (TxB2) formation induced by collagen have been examined in vitro. Platelets from two species, man and the rat, have been used. In man, aspirin and CHI abolished TxB2 production but only partially inhibited aggregation. CP/CPK partially inhibited aggregation and TxB2 formation. In the rat, aspirin and CHI abolished TxB2 formation but had no effect on aggregation. CP/CPK completely inhibited aggregation and partially inhibited TxB2 generation. In man, collagen-induced aggregation is largely dependent on ADP and to a lesser extent on arachidonate metabolites whereas, in the rat, ADP alone mediates aggregation induced by this agonist. The results with CP/CPK suggest that TxB2 formation is dependent either on the prior release of platelet ADP or on aggregation itself rather than being responsible for the aggregation response.
已在体外研究了阿司匹林、羧基庚基咪唑(CHI)以及磷酸肌酸/肌酸磷酸激酶(CP/CPK)对胶原诱导的血小板聚集和血栓素B2(TxB2)形成的影响。使用了两种物种(人类和大鼠)的血小板。在人类中,阿司匹林和CHI可消除TxB2的产生,但仅部分抑制聚集。CP/CPK部分抑制聚集和TxB2的形成。在大鼠中,阿司匹林和CHI可消除TxB2的形成,但对聚集无影响。CP/CPK完全抑制聚集并部分抑制TxB2的产生。在人类中,胶原诱导的聚集很大程度上依赖于ADP,在较小程度上依赖于花生四烯酸代谢产物,而在大鼠中,仅ADP介导该激动剂诱导的聚集。CP/CPK的研究结果表明,TxB2的形成要么依赖于血小板ADP的预先释放,要么依赖于聚集本身,而不是聚集反应的原因。