Okuma M, Takayama H, Sugiyama T, Sensaki S, Uchino H
Thromb Haemost. 1982 Dec 27;48(3):330-3.
The effects of etamsylate on human platelet aggregation and ATP release as well as on the arachidonate metabolism by the platelet have been studied. Etamsylate enhanced these platelet functions induced by arachidonic acid (AA), thromboxane A2, collagen and calcium ionophore A23187 but not those induced by ADP and epinephrine. In experiments with cyclooxygenase-inhibited platelets, AA-induced platelet aggregation was completely inhibited and it was not enhanced by etamsylate, while A23187-induced aggregation was partially inhibited and this aggregation was enhanced by etamsylate. Platelet AA metabolism including thrombin-induced AA liberation from phospholipids as well as the lipoxygenase and cyclo-oxygenase pathways was not significantly affected by etamsylate. These results suggested that etamsylate enhanced platelet response to thromboxane A2 and calcium ionophore and that this could be included as a mechanism for its potentiating effect on platelet functions.
已对酚磺乙胺对人血小板聚集、ATP释放以及血小板花生四烯酸代谢的影响进行了研究。酚磺乙胺增强了由花生四烯酸(AA)、血栓素A2、胶原和钙离子载体A23187诱导的这些血小板功能,但未增强由ADP和肾上腺素诱导的血小板功能。在使用环氧化酶抑制的血小板进行的实验中,AA诱导的血小板聚集被完全抑制,且酚磺乙胺未增强该聚集,而A23187诱导的聚集被部分抑制,且酚磺乙胺增强了该聚集。包括凝血酶诱导的AA从磷脂中释放以及脂氧合酶和环氧化酶途径在内的血小板AA代谢未受到酚磺乙胺的显著影响。这些结果表明,酚磺乙胺增强了血小板对血栓素A2和钙离子载体的反应,且这可被视为其对血小板功能具有增强作用的一种机制。