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大鼠纤溶、血清素和血小板聚集的应激依赖性变化。

Stress-dependent changes in fibrinolysis, serotonin and platelet aggregation in rats.

作者信息

Malyszko J, Urano T, Takada Y, Takada A

机构信息

Department of Physiology, Hamamatsu University School of Medicine, Shizuoka, Japan.

出版信息

Life Sci. 1994;54(17):1275-80. doi: 10.1016/0024-3205(94)00855-8.

Abstract

The effects of different kinds of acute stress on collagen-induced whole blood platelet aggregation and fibrinolysis in relation to blood serotonergic measures were studied. In rats water-immersion restraint stress resulted in a shortening of euglobulin clot lysis time (ECLT), an increase in tissue plasminogen activator (tPA) activity with a concurrent fall in its inhibitor activity. Footshock caused rather a suppression in fibrinolysis with a prolongation of ECLT and a decline in tPA activity as well as a reduction in whole blood platelet aggregation induced by collagen. Serotonin (5-HT) level, a marker of a severity of stress, increased after footshock application with a concomitant rise in its major metabolite-5-hydroxyindoleacetic acid (5-HIAA). This indicates an enhanced 5-HT metabolism. Following water-immersion restraint stress 5-HT and 5-HIAA levels did not differ from controls. In both groups of stressed animals an inverse correlation between tPA activity and blood serotonin was observed. Our data indicate that these types of stress may influence either fibrinolysis or peripheral serotonergic mechanism in different ways. Acute and severe stress such as footshock by causing an impairment in fibrinolysis and a rise in 5-HT may contribute to the pathogenesis of thrombosis and henceforth to the development of atherosclerosis.

摘要

研究了不同类型的急性应激对胶原诱导的全血血小板聚集和纤维蛋白溶解的影响,并将其与血液中血清素能指标相关联。在大鼠中,水浸束缚应激导致优球蛋白凝块溶解时间(ECLT)缩短,组织纤溶酶原激活物(tPA)活性增加,同时其抑制物活性下降。足部电击则导致纤维蛋白溶解受到抑制,ECLT延长,tPA活性降低,以及胶原诱导的全血血小板聚集减少。血清素(5-HT)水平作为应激严重程度的标志物,在施加足部电击后升高,同时其主要代谢产物5-羟吲哚乙酸(5-HIAA)也随之升高。这表明5-HT代谢增强。水浸束缚应激后,5-HT和5-HIAA水平与对照组无差异。在两组应激动物中,均观察到tPA活性与血液血清素之间呈负相关。我们的数据表明,这些类型的应激可能以不同方式影响纤维蛋白溶解或外周血清素能机制。急性和严重应激,如足部电击,通过导致纤维蛋白溶解受损和5-HT升高,可能促成血栓形成的发病机制,进而导致动脉粥样硬化的发展。

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