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右旋糖酐诱导的人体类过敏反应:高分子量激肽原的反应性改变

Dextran-induced anaphylactoid reaction in man: altered reactivity of high molecular weight kininogen.

作者信息

Briseid G, Briseid K

出版信息

Acta Pharmacol Toxicol (Copenh). 1980 Aug;47(2):119-26. doi: 10.1111/j.1600-0773.1980.tb01850.x.

Abstract

Normal levels of factor XII and of high and low molecular weight kininogens (HMWK and LMWK) were registered in plasma specimens from 5 individuals who had developed anaphylactoid reactions upon injection of dextran during surgery (dextran reactors, DR). Factor XII was assayed as prekallikrein activator (PKA) activated with kaolin at 0 degrees, and kininogen fractions were estimated through the release of kinin caused by plasma kallikrein or hog pancreas kallikrein (HPK). Subnormal levels of factor XII apparently present in plasma from one DR, and after affinity chromatography on a lysine-Sepharose column also in plasma from another DR, were normalized by addition of plasma deficient in factor XII or by addition of purified HMWK. Treatment of plasma from DR with acetone (25% v/v) induced a conversion of HMWK into a state which was non-functional as a cofactor in the surface-dependent activation of factor XII, and the passage of plasma from DR through a lysine-Sepharose column altered the HMWK present to a substance that released kinin only very slowly by incubation with HPK. It is concluded that the treatments mentioned will favour the activation in plasma from DR of a factor that will cause the conversion of HMWK. Previous experiments with rat plasma demonstrated that plasmin and also a plasmin-like factor without affinity for lysine-Sepharose were able to destroy the capacity of HMWK to function as a cofactor in the surface-dependent activation of factor XII, without a corresponding release of kinin.

摘要

在5名手术期间注射葡聚糖后发生类过敏反应的个体(葡聚糖反应者,DR)的血浆样本中,检测到因子XII以及高分子量激肽原和低分子量激肽原(HMWK和LMWK)的水平正常。因子XII作为在0℃用高岭土激活的前激肽释放酶激活剂(PKA)进行测定,激肽原组分通过血浆激肽释放酶或猪胰激肽释放酶(HPK)引起的激肽释放来估计。一名DR的血浆中明显存在的因子XII水平低于正常,在赖氨酸-琼脂糖柱上进行亲和层析后,另一名DR的血浆中也是如此,通过添加缺乏因子XII的血浆或添加纯化的HMWK可使其恢复正常。用丙酮(25% v/v)处理DR的血浆会导致HMWK转化为一种状态,该状态在因子XII的表面依赖性激活中作为辅因子无功能,并且DR的血浆通过赖氨酸-琼脂糖柱会使存在的HMWK改变为一种与HPK孵育时仅非常缓慢释放激肽的物质。得出的结论是,上述处理将有利于DR血浆中一种导致HMWK转化的因子的激活。先前对大鼠血浆的实验表明,纤溶酶以及对赖氨酸-琼脂糖柱无亲和力的类纤溶酶因子能够破坏HMWK在因子XII的表面依赖性激活中作为辅因子的功能,而不会相应地释放激肽。

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