Reimers H J, Scharf R E, Baker R K
Blood. 1984 Apr;63(4):858-65.
Exposure of horse platelets to thrombin has been reported to cause nearly complete inactivation of cyclooxygenase within 30 sec. This contrasts with the observation that human platelets, depleted of their granule constituents by stimulation with thrombin, still aggregate in response to arachidonic acid, a reaction presumably mediated by thromboxane A2 (TxA2) formation. Because of this conflicting evidence, TxA2 formation was measured by radioimmunoassay in washed human platelets depleted of their alpha- and dense-storage granule constituents by prior stimulation with thrombin. These platelets aggregated in response to adenosine diphosphate (ADP), collagen, arachidonic acid, and thrombin, and formed TxA2. However, collagen- and thrombin-induced TxA2 formation by these platelets was reduced in comparison to control platelets that had not been depleted of their storage granule constituents by prior thrombin stimulation. In contrast, arachidonic acid-induced TxA2 formation was not significantly different in thrombin-depleted and control platelets. These results demonstrate that thrombin can induce degranulation of platelets without concomitant inactivation of cyclooxygenase.
据报道，将马血小板暴露于凝血酶中会在30秒内导致环氧化酶几乎完全失活。这与以下观察结果形成对比：人血小板在被凝血酶刺激耗尽其颗粒成分后，仍会对花生四烯酸产生聚集反应，该反应可能由血栓素A2（TxA2）的形成介导。由于存在这种相互矛盾的证据，因此通过放射免疫分析法对经凝血酶预先刺激而耗尽其α-颗粒和致密储存颗粒成分的洗涤人血小板中的TxA2形成进行了测定。这些血小板对二磷酸腺苷（ADP）、胶原蛋白、花生四烯酸和凝血酶产生聚集反应，并形成TxA2。然而，与未通过凝血酶预先刺激耗尽其储存颗粒成分的对照血小板相比，这些血小板由胶原蛋白和凝血酶诱导的TxA2形成减少。相比之下，花生四烯酸诱导的TxA2形成在凝血酶耗尽的血小板和对照血小板中没有显著差异。这些结果表明，凝血酶可诱导血小板脱颗粒，而不会同时使环氧化酶失活。
