Siffert W, Fox G, Gros G
Biochem Biophys Res Commun. 1984 May 31;121(1):266-70. doi: 10.1016/0006-291x(84)90717-4.
We have studied the effect of ethoxzolamide , a specific carbonic anhydrase inhibitor, on the velocity of thrombin-stimulated platelet aggregation. After preincubation of platelet rich plasma with 10(-6) M ethoxzolamide the velocity of platelet aggregation was reduced by about 40%. Between 10(-11) M and 10(-10)M ethoxzolamide was necessary to achieve a half-maximal diminution of the aggregation velocity. An identical maximal reduction of the velocity of aggregation as with ethoxzolamide could be achieved by a nearly complete removal of CO2 from the platelet rich plasma. These results suggest that the intracellular CO2 hydration-dehydration reaction is involved in the activation of human platelets by thrombin. It is possible that the cytosolic carbonic anhydrase of platelets provides a rapid source of the protons that are transferred across the plasma membrane during the activation process.
我们研究了特异性碳酸酐酶抑制剂乙氧唑胺对凝血酶刺激的血小板聚集速度的影响。用10^(-6)M乙氧唑胺预孵育富血小板血浆后，血小板聚集速度降低了约40%。在10^(-11)M至10^(-10)M之间的乙氧唑胺浓度是使聚集速度减半所需的浓度。通过几乎完全去除富血小板血浆中的二氧化碳，可以实现与乙氧唑胺相同程度的聚集速度最大降低。这些结果表明，细胞内二氧化碳的水合-脱水反应参与了凝血酶对人血小板的激活。血小板胞质碳酸酐酶有可能提供质子的快速来源，这些质子在激活过程中跨质膜转移。
