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本文观察了新型强心剂咪苯嗪酮(Cl-914)对血小板聚集、血栓形成和血小板cAMP含量的影响。用比浊法测定Cl-914体外抑制AA,ADP和胶原诱导兔血小板聚集的IC_(50),分别为2.6,8.9和15.8μM;大鼠iv Cl-914 1.25mg/kg能抑制实验性血栓形成,20 mg/kg能抑制上述三种诱导剂引起的血小板聚集。在体外,用竞争性蛋白结合法测定,CI-914可使洗涤兔血小板cAMP含量明显升高。CI-914能以剂量依赖方式协同PGE_1抑制血小板聚集和升高血小板cAMP的含量。提示CI-914升高血小板cAMP含量可能是其抑制血小板聚集和抗血栓形成的主要机理。
This article investigates the effect of a new cardiotonic agent, imidacloprid (Cl-914), on platelet aggregation, thrombosis, and platelet cAMP levels. The IC50 of platelet aggregation induced by Cl-914 in vitro was detected by turbidimetry in 2.6, 8.9 and 15.8 μM for AA, ADP and collagen, respectively. The rat iv Cl-914 1.25 mg / kg inhibited the formation of experimental thrombosis , 20 mg / kg can inhibit platelet aggregation induced by the above three inducing agents. In vitro, the competitive protein binding assay, CI-914 can significantly increase the cAMP content of washed rabbit platelets. CI-914 synergizes with PGE 1 to inhibit platelet aggregation and increase platelet cAMP in a dose-dependent manner. It is suggested that elevated cAMP content of platelet in CI-914 may be the main mechanism of its inhibition of platelet aggregation and anti-thrombosis.