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血小板条带。II. 凝血酶激活的人血小板中的药物机械偶联

The platelet strip. II. Pharmacomechanical coupling in thrombin-activated human platelets.

作者信息

Salganicoff L, Sevy R W

出版信息

Am J Physiol. 1985 Sep;249(3 Pt 1):C288-96. doi: 10.1152/ajpcell.1985.249.3.C288.

DOI:10.1152/ajpcell.1985.249.3.C288
PMID:2994486
Abstract

A model of contracted, irreversibly aggregated thrombin-activated human platelets relaxes when treated with ethyleneglycol-bis(beta-aminoethylether-N,N'-tetraacetic acid (EGTA) in the presence of Mg2+. Inhibition of the cyclooxygenase or blockade of the thromboxane A2 receptor decreases the tension partially, but EGTA treatment is needed for full relaxation. After a stable relaxation has been achieved (3-4 h), Ca2+ addition in a cumulative manner does not reinduce contraction. Whether in the absence or presence of external Ca2+, the relaxed preparation contracts when stimulated with ADP, epinephrine, thromboxane A2 or its analogues, or thrombin. At supramaximal doses, each of the agonists activates only a partial amount of the total tension capable of being generated. Addition of an agonist of a different class to the partially contracted preparation further increases its force. The contractile responses are reversible on washout, with kinetics dependent on the class of agonist and time of contact with the preparation. The contraction induced by the prolonged simultaneous stimulation with ADP, arachidonate, and thrombin reverts very slowly on washout of the agonists and for all practical purposes reproduces the initial state of irreversible platelet contraction.

摘要

一种收缩的、不可逆聚集的凝血酶激活的人血小板模型,在Mg2+存在的情况下用乙二醇双(β-氨基乙基醚)-N,N'-四乙酸(EGTA)处理时会松弛。环氧合酶的抑制或血栓素A2受体的阻断会部分降低张力,但完全松弛需要EGTA处理。在达到稳定松弛(3-4小时)后,以累积方式添加Ca2+不会再次诱导收缩。无论是否存在外部Ca2+,当用ADP、肾上腺素、血栓素A2或其类似物或凝血酶刺激时,松弛的制剂都会收缩。在超最大剂量下,每种激动剂仅激活能够产生的总张力的一部分。向部分收缩的制剂中添加不同类别的激动剂会进一步增加其力量。收缩反应在洗脱时是可逆的,动力学取决于激动剂的类别和与制剂接触的时间。由ADP、花生四烯酸和凝血酶长时间同时刺激引起的收缩在激动剂洗脱时恢复非常缓慢,实际上再现了血小板不可逆收缩的初始状态。

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The platelet strip. II. Pharmacomechanical coupling in thrombin-activated human platelets.血小板条带。II. 凝血酶激活的人血小板中的药物机械偶联
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