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激肽与溶栓

Kinins and thrombolysis.

作者信息

Swies J, Chłopicki S, Gryglewski R J

机构信息

Department of Pharmacology, University School of Medicine, Kraków, Poland.

出版信息

J Physiol Pharmacol. 1993 Jun;44(2):171-7.

PMID:8358053
Abstract

In cats with extracorporeal circulation arterial blood pressure and thrombolysis were assayed. In this model apart from their hypotensive properties kallikrein (3-10 units/kg, i.v.) and captopril (> 200 micrograms/kg, i.v.) dissipated blood clots which were preformed on superfused collagen strips. Captopril at a lower dose of 50 micrograms/kg i.v. potentiated the thrombolytic effect of kallikrein while aprotinin (100,000 unit/kg, i.v.) abolished it. Thrombolysis by kallikrein was mediated by an unstable principle which was decomposed by blood during 15 min of incubation at 37 degrees C. Generation of this principle was inhibited by pretreatment of animals with aspirin (50 mg/kg, i.v.). The above analysis points to prostacyclin which owing to its platelet-suppressant and fibrinolytic properties induces thrombolysis when released by kinins.

摘要

在进行体外循环的猫身上测定动脉血压和溶栓情况。在该模型中,除了具有降压特性外,激肽释放酶(3 - 10单位/千克,静脉注射)和卡托普利(>200微克/千克,静脉注射)能溶解预先形成于灌注胶原条上的血凝块。静脉注射较低剂量50微克/千克的卡托普利可增强激肽释放酶的溶栓作用,而抑肽酶(100,000单位/千克,静脉注射)则可消除这种作用。激肽释放酶的溶栓作用由一种不稳定物质介导,该物质在37℃孵育15分钟期间会被血液分解。用阿司匹林(50毫克/千克,静脉注射)预处理动物可抑制这种物质的生成。上述分析表明是前列环素,由于其抑制血小板和纤溶特性,当由激肽释放时可诱导溶栓。

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