Glass F, Lippton H, Kadowitz P J
Thromb Haemost. 1981 Dec 23;46(4):676-9.
The effects of methylprednisolone and hydrocortisone on platelet aggregation induced by arachidonic acid (AA), collagen, adenosine diphosphate (ADP), prostaglandin (PG) H2, and a stable PGH2 analog, were studied in platelet-rich plasma (PRP) from the rabbit. Incubation of either steroid in PRP inhibited AA-, collagen- and ADP-induced platelet aggregation in a concentration-related manner. The dose of methylprednisolone required to inhibit 0.02 mM AA-induced aggregation was lower than that required to inhibit either 0.08 microgram/ml collagen or 0.2 microM ADP-induced aggregation. Methylprednisolone produced a dose-dependent inhibition of platelet aggregation induced by PGH2 and the stable PGH2 analog. In washed platelets methylprednisolone was more effective in inhibiting AA-induced aggregation than ADP- or collagen-induced aggregation; however, the difference in effect was less than in PRP. Platelet responses to AA in PRP from rabbits treated with hydrocortisone or methylprednisolone, 100 mg/kg i.v., were inhibited in a transient manner, whereas aggregation induced by ADP under similar conditions was unchanged. Since inhibition of aggregation elicited by AA occurred at concentrations which do not influence PGH2-, PGH2 analog-, collagen- or ADP-induced aggregation, the present data suggest that the steroids may inhibit the incorporation, the release, or the metabolism of arachidonic acid in platelets. The actual mechanism of this relatively specific inhibition of AA-induced aggregation by anti-inflammatory steroids is uncertain but may be related to the membrane "stabilizing" properties of methylprednisolone and hydrocortisone.
在兔富血小板血浆（PRP）中研究了甲基泼尼松龙和氢化可的松对花生四烯酸（AA）、胶原、二磷酸腺苷（ADP）、前列腺素（PG）H2以及一种稳定的PGH2类似物诱导的血小板聚集的影响。在PRP中孵育这两种类固醇均可浓度依赖性地抑制AA、胶原和ADP诱导的血小板聚集。抑制0.02 mM AA诱导的聚集所需的甲基泼尼松龙剂量低于抑制0.08微克/毫升胶原或0.2 microM ADP诱导的聚集所需的剂量。甲基泼尼松龙对PGH2和稳定的PGH2类似物诱导的血小板聚集产生剂量依赖性抑制。在洗涤过的血小板中，甲基泼尼松龙抑制AA诱导的聚集比抑制ADP或胶原诱导的聚集更有效；然而，效果差异小于在PRP中的情况。静脉注射100 mg/kg氢化可的松或甲基泼尼松龙处理的兔的PRP中血小板对AA的反应被短暂抑制，而在类似条件下ADP诱导的聚集未改变。由于在不影响PGH2、PGH2类似物、胶原或ADP诱导的聚集的浓度下发生了对AA诱导的聚集的抑制，目前的数据表明类固醇可能抑制血小板中花生四烯酸的掺入、释放或代谢。抗炎类固醇对AA诱导的聚集这种相对特异性抑制的实际机制尚不确定，但可能与甲基泼尼松龙和氢化可的松的膜“稳定”特性有关。
