Literature DB >> 8287866

The mechanism of myocyte death in ischaemia.

L H Opie1.   

Abstract

Mechanisms of myocyte cell death in severe ischaemia may include: (1) accumulated metabolic products; (2) activation of membrane phospholipases; (3) formation of oxygen-derived free-radicals; (4) infiltration by activated neutrophils; (5) increased circulating catecholamines; (6) cytosolic calcium overload; (7) an inadequate supply of glycolytically produced ATP. The hypothesis is proposed that failure of glycolysis leads to inadequate control of intracellular calcium, which is a lethal event. This hypothesis would explain the concept that in the hibernating myocardium, viable zones can be detected by positron emission tomography of fluoro-deoxyglucose.

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Year:  1993        PMID: 8287866     DOI: 10.1093/eurheartj/14.suppl_g.31

Source DB:  PubMed          Journal:  Eur Heart J        ISSN: 0195-668X            Impact factor:   29.983


  6 in total

1.  The role of myocardial glycogen content for the development of isoprenaline-induced myocardial lesions in different inbred strains of rats.

Authors:  M Mráz; V Kren; D Krsiaková; A Vrána; S Hynie
Journal:  Basic Res Cardiol       Date:  1995 Nov-Dec       Impact factor: 17.165

2.  Heart glycogen content and isoprenaline-induced myocardial lesions.

Authors:  M Mráz; S Hynie
Journal:  Mol Cell Biochem       Date:  1996 Oct-Nov       Impact factor: 3.396

Review 3.  Functional Impact of Ryanodine Receptor Oxidation on Intracellular Calcium Regulation in the Heart.

Authors:  Aleksey V Zima; Stefan R Mazurek
Journal:  Rev Physiol Biochem Pharmacol       Date:  2016       Impact factor: 5.545

Review 4.  Nitroimidazoles and imaging hypoxia.

Authors:  A Nunn; K Linder; H W Strauss
Journal:  Eur J Nucl Med       Date:  1995-03

5.  Perturbations in cardiac metabolism in a human model of acute myocardial ischaemia.

Authors:  Sanoj Chacko; Mamas A Mamas; Magdi El-Omar; David Simon; Sohaib Haseeb; Farzin Fath-Ordoubadi; Bernard Clarke; Ludwig Neyses; Warwick B Dunn
Journal:  Metabolomics       Date:  2021-08-23       Impact factor: 4.290

6.  Deletion of Apoptosis Inhibitor of Macrophage (AIM)/CD5L Attenuates the Inflammatory Response and Infarct Size in Acute Myocardial Infarction.

Authors:  Toshiyuki Nishikido; Jun-ichi Oyama; Aya Shiraki; Hiroshi Komoda; Koichi Node
Journal:  J Am Heart Assoc       Date:  2016-04-04       Impact factor: 5.501

  6 in total

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