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低密度脂蛋白增强了人体血浆中血小板对血清素的反应。

Low-density lipoprotein amplifies the platelet response to serotonin in human plasma.

作者信息

Fetkovska N, Fedelesova V, Dzurik R

机构信息

Clinic of Pharmacotherapy, Medical Bionics Research Institute, Bratislava, Czechoslovakia.

出版信息

J Hypertens Suppl. 1989 Dec;7(6):S164-5. doi: 10.1097/00004872-198900076-00078.

Abstract

The effect of low-density lipoprotein, serotonin and low-density lipoprotein plus serotonin on platelet aggregation (measured ex vivo in plasma) was studied in 28 normotensive subjects (15 non-smokers, 13 smokers) and 15 previously untreated non-smoking patients with essential hypertension. Low-density lipoprotein alone had no platelet-activating effect. Serotonin-induced platelet aggregation was enhanced by low-density lipoprotein in both the normotensive and the hypertensive subjects. The platelet response to low-density lipoprotein plus serotonin was higher in the smokers than in the non-smokers; it was also higher in the hypertensive patients than in the normotensive controls. We conclude that low-density lipoprotein activates platelets in plasma via an interaction with a serotonergic mechanism. Low-density lipoprotein amplifies the serotonin-induced platelet aggregation (normally reversible), making it irreversible. A higher platelet response to low-density lipoprotein plus serotonin in patients with essential hypertension may be of pathophysiological relevance in respect to the thrombovascular lesions accompanying hypertension and/or atherosclerosis.

摘要

在28名血压正常的受试者(15名不吸烟者,13名吸烟者)和15名未经治疗的原发性高血压不吸烟患者中,研究了低密度脂蛋白、血清素以及低密度脂蛋白加血清素对血小板聚集(在血浆中离体测量)的影响。单独的低密度脂蛋白没有血小板激活作用。在血压正常和高血压受试者中,血清素诱导的血小板聚集均因低密度脂蛋白而增强。吸烟者对低密度脂蛋白加血清素的血小板反应高于不吸烟者;高血压患者的反应也高于血压正常的对照组。我们得出结论,低密度脂蛋白通过与血清素能机制相互作用激活血浆中的血小板。低密度脂蛋白放大了血清素诱导的血小板聚集(通常是可逆的),使其变为不可逆。原发性高血压患者对低密度脂蛋白加血清素的血小板反应较高,这可能与高血压和/或动脉粥样硬化伴随的血栓血管病变具有病理生理学相关性。

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