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氯丙嗪和阿米替林对离体犬基底动脉及人血小板的反应。

Responses of isolated canine basilar artery and human platelet to chlorpromazine and amitriptyline.

作者信息

Sukenaga A, Tani E, Fukumori T, Maeda Y

出版信息

Stroke. 1984 Mar-Apr;15(2):295-300. doi: 10.1161/01.str.15.2.295.

Abstract

Sustained contraction of isolated canine basilar artery was induced by addition of prostaglandin F2 alpha, prostaglandin E2, hemoglobin-containing solution, or serum. Human platelet aggregation was induced by 1.0 microM adenosine diphosphate. The sustained contraction of basilar artery and the aggregation of platelet, particularly its secondary aggregation, were inhibited in a dose-dependent manner by addition of chlorpromazine or amitriptyline; calmodulin antagonist. The molar concentrations at 50% inhibition by chlorpromazine or amitriptyline were 5.9 to 7.7 microM or 28 to 39 microM for the contraction of basilar artery and 57 microM or 111 microM for the secondary aggregation of platelet. The results were discussed mainly on the basis of interaction of psychotropic drugs and Ca2+, calmodulin-dependent enzymes, particularly myosin light chain phosphorylation.

摘要

添加前列腺素F2α、前列腺素E2、含血红蛋白溶液或血清可诱导离体犬基底动脉持续收缩。1.0微摩尔二磷酸腺苷可诱导人血小板聚集。添加氯丙嗪或阿米替林(钙调蛋白拮抗剂)后,基底动脉的持续收缩和血小板聚集,尤其是其继发性聚集,均呈剂量依赖性受到抑制。氯丙嗪或阿米替林对基底动脉收缩的50%抑制摩尔浓度分别为5.9至7.7微摩尔或28至39微摩尔,对血小板继发性聚集的抑制摩尔浓度分别为57微摩尔或111微摩尔。主要基于精神药物与Ca2+、钙调蛋白依赖性酶(尤其是肌球蛋白轻链磷酸化)的相互作用对结果进行了讨论。

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