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磺吡酮与缺血性心脏病中的血小板血清素能机制

Sulphinpyrazone and the platelet serotoninergic mechanism in ischaemic heart disease.

作者信息

Puri V K, Rawat A, Sharma A, Mehrotra A, Hasan M, Shanker K, Verma M, Sinha J N, Bhargava K P

出版信息

Br Med J (Clin Res Ed). 1986 Sep 6;293(6547):591-3. doi: 10.1136/bmj.293.6547.591.

Abstract

A double blind study in 25 patients with ischaemic heart disease and 20 matched healthy controls examined the effect of sulphinpyrazone on the uptake of serotonin by platelets and the basal concentrations of serotonin in platelets. Uptake was measured using tritium labelled serotonin and basal concentrations estimated spectrophotofluorometrically. Serotonin uptake was significantly increased both in the patients with chronic stable angina of effort and in those with a history of myocardial infarction six months or more previously. Sulphinpyrazone reduced serotonin uptake from 94.25 (SE 8.65) to 57.86 (5.37) cpm/10(8) platelets after 24 weeks of treatment in the group with stable angina and from 137.45 (16.26) to 68.08 (8.38) cpm/10(8) platelets in the myocardial infarction group. Raised basal concentrations in the two groups were also reduced by sulphinpyrazone. Placebo had no effect on serotonin uptake or basal concentrations in either group of patients. The ability of sulphinpyrazone to inhibit uptake and reduce basal concentrations of serotonin in patients with ischaemic heart disease may be yet another mechanism through which this drug exerts its beneficial antiplatelet effect.

摘要

一项针对25名缺血性心脏病患者和20名匹配的健康对照者的双盲研究,检测了磺吡酮对血小板摄取5-羟色胺的影响以及血小板中5-羟色胺的基础浓度。摄取量用氚标记的5-羟色胺进行测量,基础浓度用分光荧光法估算。在慢性稳定劳力型心绞痛患者以及六个月或更久之前有心肌梗死病史的患者中,5-羟色胺摄取均显著增加。在稳定型心绞痛组,经过24周治疗后,磺吡酮使5-羟色胺摄取从94.25(标准误8.65)降至57.86(5.37)cpm/10⁸血小板;在心肌梗死组,从137.45(16.26)降至68.08(8.38)cpm/10⁸血小板。两组中升高的基础浓度也因磺吡酮而降低。安慰剂对两组患者的5-羟色胺摄取或基础浓度均无影响。磺吡酮抑制缺血性心脏病患者摄取5-羟色胺并降低其基础浓度的能力,可能是该药发挥有益抗血小板作用的又一机制。

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