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糖原磷酸化酶同工酶BB在心肌缺血性损伤和梗死诊断中的应用

Glycogen phosphorylase isoenzyme BB in diagnosis of myocardial ischaemic injury and infarction.

作者信息

Krause E G, Rabitzsch G, Noll F, Mair J, Puschendorf B

机构信息

Department of Molecular Cardiology, Max Delbrück Center for Molecular Medicine, Berlin-Buch, Germany.

出版信息

Mol Cell Biochem. 1996 Jul-Aug;160-161:289-95. doi: 10.1007/BF00240061.

Abstract

This review deals with glycogen phosphorylase (GP) and its isoenzyme BB in the diagnosis of ischaemic myocardial injury. Early identification and confirmation of acute myocardial infarction is essential for correct patient care and disposition decision in the emergency department. In this respect, glycogen phosphorylase isoenzyme BB (GPBB) based on its metabolic function is an enzyme for early laboratory detection of ischaemia. In the aerobic heart muscle GPBB together with glycogen is tightly associated with the vesicles of the sarcoplasmic reticulum. Release of GPBB, the main isoform in the human myocardium, essentially depends on the degradation of glycogen, which is catalyzed by GP. Ischaemia is known to favour the conversion of bound GP in the b form into GP a, thereby accelerating glycogen breakdown, which is the ultimate prerequisite for getting GP into a soluble form being able to move freely in the cytosol. The efflux of GPBB into the extracellular fluid follows if ischaemia-induced structural alterations in the cell membrane become manifest. The clinical application of GPBB as a marker of ischaemic myocardial injury is a very promising tool for extending our knowledge of the severity of myocardial ischaemic events in the various coronary syndromes. The rational roots of this development were originated from Albert Wollenberger's research work on the biochemistry of cardiac ischaemia and the transient acceleration of glycogenolysis mainly brought about by GP activation.

摘要

本综述探讨糖原磷酸化酶(GP)及其同工酶BB在缺血性心肌损伤诊断中的应用。早期识别和确诊急性心肌梗死对于急诊科正确的患者护理和处置决策至关重要。在这方面,基于其代谢功能的糖原磷酸化酶同工酶BB(GPBB)是一种用于缺血早期实验室检测的酶。在有氧心肌中,GPBB与糖原一起紧密地与肌浆网小泡结合。人心肌中的主要同工型GPBB的释放主要取决于糖原的降解,而糖原降解由GP催化。已知缺血有利于将结合形式的b型GP转化为a型GP,从而加速糖原分解,这是使GP进入能够在细胞质中自由移动的可溶形式的最终前提条件。如果细胞膜中缺血诱导的结构改变显现出来,GPBB就会外流到细胞外液中。GPBB作为缺血性心肌损伤标志物的临床应用是一个非常有前景的工具,有助于我们了解各种冠状动脉综合征中心肌缺血事件的严重程度。这一进展的合理根源源于阿尔伯特·沃伦伯格关于心脏缺血生物化学以及主要由GP激活引起的糖原分解短暂加速的研究工作。

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