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原发性高血压或脑血管疾病患者的血栓素生成及口服阿司匹林的作用

Thromboxane generation in patients with essential hypertension or cerebrovascular disease and effect of oral aspirin.

作者信息

Matsumoto M, Nukada T, Uyama O, Yoneda S, Imaizumi M, Miyamoto T, Kayama N

出版信息

Thromb Haemost. 1980 Aug 29;44(1):16-22.

PMID:7423441
Abstract

The ability of platelets to synthesize thromboxane B2 (TxB2) from arachidonic acid (AA) or prostaglandin H2 (PGH2) was studied in 26 control subjects, 40 patients with essential hypertension, 20 patients with cerebrovascular disease (CVD) not taking aspirin and 11 patients with CVD taking aspirin. The activity of platelets to form TxB2 from AA or PGH2 was measured using 1-14C arachidonic acid or 1-14C PGH2 as a substrate. There was no significant difference in TxB2 generation from AA or PGH2 among the platelets collected from the control subjects, hypertensive patients and CVD patients not taking aspirin. In CVD patients taking aspirin, marked suppression was observed in TxB2 synthesis from AA, but no suppression in TxB2 synthesis from PGH2. At least 750 mg aspirin per day were required for nearly complete suppression of TxB2 generation from AA.

摘要

在26名对照受试者、40名原发性高血压患者、20名未服用阿司匹林的脑血管疾病(CVD)患者和11名服用阿司匹林的CVD患者中,研究了血小板从花生四烯酸(AA)或前列腺素H2(PGH2)合成血栓素B2(TxB2)的能力。以1-14C花生四烯酸或1-14C PGH2为底物,测量血小板从AA或PGH2形成TxB2的活性。在对照受试者、高血压患者和未服用阿司匹林的CVD患者采集的血小板中,从AA或PGH2生成TxB2没有显著差异。在服用阿司匹林的CVD患者中,观察到从AA合成TxB2受到明显抑制,但从PGH2合成TxB2没有受到抑制。每天至少需要750毫克阿司匹林才能几乎完全抑制从AA生成TxB2。

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