Pipili E
Thromb Haemost. 1985 Oct 30;54(3):645-9.
The role of membrane potential in the activation of human platelets by thrombin, ADP and PAF was assessed, using the fluorescent probe diSC3(5). Thrombin, ADP and PAF transiently depolarised the platelet membrane by 6-8 mV from its resting level (-70 mV). This depolarisation had a similar time course to that of shape change. The ionophores valinomycin and gramicidin hyperpolarised and depolarised the platelets respectively but did not activate them. In contrast, exposure of platelets to high K+ media both depolarised and caused them to change shape. Removal of Na+ from the suspension media abolished the depolarisation induced by thrombin, ADP and PAF but the platelets under these conditions were still capable of changing shape and aggregating. This result indicates that the observed depolarisation depends on Na+ fluxes. Amiloride or tetrodotoxin did not mimic the effect of Na+ removal suggesting that any Na+ movement involved does not go through the classic "Na+ channel". Thrombin, ADP and PAF still depolarised the platelet membrane in the absence of added Ca++. Under these conditions, however, the membrane did not repolarise. It is evident that all three agents, thrombin, ADP and PAF, change the membrane potential of human washed platelets through a similar mechanism and this change seems to be a consequence of stimulus-receptor interaction (and platelet activation?). A causal relationship however between these events cannot be clearly shown.
利用荧光探针diSC3(5)评估了膜电位在凝血酶、二磷酸腺苷（ADP）和血小板活化因子（PAF）激活人血小板过程中的作用。凝血酶、ADP和PAF可使血小板膜从静息水平（-70mV）瞬间去极化6 - 8mV。这种去极化的时间进程与形态变化相似。离子载体缬氨霉素和短杆菌肽分别使血小板超极化和去极化，但未激活血小板。相反，将血小板暴露于高钾培养基中会使其去极化并导致形态改变。从悬浮培养基中去除钠离子可消除凝血酶、ADP和PAF诱导的去极化，但在此条件下血小板仍能改变形态并聚集。这一结果表明，观察到的去极化依赖于钠离子通量。氨氯吡咪或河豚毒素不能模拟去除钠离子的效果，这表明所涉及的任何钠离子移动并非通过经典的“钠离子通道”。在未添加钙离子的情况下，凝血酶、ADP和PAF仍能使血小板膜去极化。然而，在此条件下，膜不会复极化。显然，凝血酶、ADP和PAF这三种物质通过类似机制改变人洗涤血小板的膜电位，这种变化似乎是刺激 - 受体相互作用（以及血小板活化？）的结果。然而，这些事件之间的因果关系尚不能明确显示。
