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维拉帕米与胶原诱导的血小板反应——细胞内钙在血小板激活中作用的证据

Verapamil and collagen-induced platelet reactions--evidence for a role for intracellular calcium in platelet activation.

作者信息

Han P, Boatwright C, Ardlie N G

出版信息

Thromb Haemost. 1983 Aug 30;50(2):537-40.

PMID:6415847
Abstract

Calcium is considered to have an essential role in various platelet reactions. Using platelets preincubated with chlortetracycline, a fluorescent divalent cation indicator, and suspended in a calcium free medium, it was shown that collagen-induced intracellular calcium redistribution occurred before the platelet shape change, the release reaction and thromboxane B2 formation. Verapamil, at concentrations which affect intracellular calcium movements, inhibited intracellular calcium redistribution in platelets and the subsequent collagen-induced platelet reactions. Low concentrations of the ionophore A23187 overcame the inhibitory effect of verapamil. These experiments provide evidence that intracellular calcium mobilization is involved in the activation of platelets by collagen. Furthermore, calcium may be released from different cellular pools since platelet secretion, aggregation and thromboxane B2 formation were inhibited at lower concentrations of verapamil than was the platelet shape change.

摘要

钙被认为在各种血小板反应中起重要作用。使用预先与荧光二价阳离子指示剂金霉素预孵育并悬浮于无钙培养基中的血小板,研究表明,胶原诱导的细胞内钙重新分布发生在血小板形状改变、释放反应和血栓素B2形成之前。维拉帕米在影响细胞内钙移动的浓度下,抑制血小板内的细胞内钙重新分布以及随后的胶原诱导的血小板反应。低浓度的离子载体A23187可克服维拉帕米的抑制作用。这些实验提供了证据,表明细胞内钙动员参与了胶原对血小板的激活。此外,钙可能从不同的细胞池释放,因为与血小板形状改变相比,较低浓度的维拉帕米就能抑制血小板分泌、聚集和血栓素B2形成。

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