内毒素所致DIC时血小板胞浆Ca^(2+)浓度变化的研究

Study on the Changes of [ Ca^(2+) ]i of Platelets in DIC Inducde by Endotoxin

本实验观察内毒素在体外对兔血小板胞浆游离钙浓度[Ca^(2+)]i的作用以及用二次注射内毒素法复制DIC模型时对[Ca^(2+)]i的影响。结果表明静息血小板[Ca^(2+)]i为112±24 nM,内毒素可直接作用于血小板,使[Ca^(2+)]i呈剂量依赖性升高。内毒素致DIG时(Ca^(2+)]i可升高三倍。结果提示内毒素可能是通过升高血小板[Ca^(2+)]i而激活血小板。血小板的激活可能是导致DIC的重要发病机制之一。

In this experiment, Disseminated Intravascular Coagulation(DIC) model was Prepared on New Zealand rabbits to observe the change of cytosolic calcium concentration [Ca2 +]i of thrombocytes measured with Quin-2 , in order to study the significance of [Ca2 +]i of thrombocytes in the occurance of endo-toxin-induced DIC. The effect of endotoxin on [Ca2+]i of platelets in vitro was also studied. The results indicated- the resting cytosolic calcium concentration of platelets of New Zealand rabbits is 112±24 nM (n= 7 ) . In vitro endotoxin can directly increase [Ca2+]i of platelet and also this effect is dose-dependent. In vivo, the experimental DIC models were prepared on New Zealand rabbits and the [Ca2+]i of platelets increase from 112 ±24 nM in normal to 343 ±48 nM, The results suggest that endotoxin can increase of [Ca2+]i of platelet in vitro and in vivo. In DIC model the platelets maintain a high level of [Ca2 +]i and result in the 'hypercoagulant' of platelet, which may be important cellular mechanism of DIC.