O'Rourke S T, Folts J D, Albrecht R M
J Lab Clin Med. 1986 Sep;108(3):206-12.
The ability of barbiturates to affect in vitro platelet aggregation of canine platelets was examined. Platelet-rich plasma was incubated with thiamylal, pentobarbital, and barbital for 10 minutes before the addition of the aggregating stimulus. All three barbiturates produced a concentration-related inhibition of platelet aggregation induced by adenosine diphosphate (ADP) and collagen. The inhibitory effect of the barbiturates could not be overcome by increasing the concentration of extracellular calcium. In contrast to ADP- and collagen-induced aggregation, no inhibitory effect was observed on aggregation initiated by A23187, 12-O-tetradecanoylphorbol-13-acetate, or phospholipase C. In further studies, the ADP-induced rise in free cytosolic calcium was blocked by the barbiturates. These findings suggest that barbiturates may interfere with the rise in internal calcium associated with agonist-receptor stimulation of platelets.
研究了巴比妥类药物对犬血小板体外聚集的影响。在添加聚集刺激物之前，将富含血小板的血浆与硫喷妥钠、戊巴比妥和巴比妥一起孵育10分钟。所有三种巴比妥类药物均对二磷酸腺苷（ADP）和胶原诱导的血小板聚集产生浓度相关的抑制作用。增加细胞外钙的浓度并不能克服巴比妥类药物的抑制作用。与ADP和胶原诱导的聚集相反，未观察到对由A23187、12-O-十四烷酰佛波醇-13-乙酸酯或磷脂酶C引发的聚集有抑制作用。在进一步的研究中，巴比妥类药物阻断了ADP诱导的游离胞质钙升高。这些发现表明，巴比妥类药物可能会干扰与血小板激动剂-受体刺激相关的细胞内钙升高。
