© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Nitric oxide, nitrates and ischaemic preconditioning
Department of Cardiology, GKT School of Medicine, KU The Rayne Institute, St.Thomas‘s Hospital, Lambeth Palace Road, London SE1 7EH, UK
* Corresponding author. Tel.: +44-171-922-8191; fax: +44-171-960-5659 m.marber@umds.ac.uk
Received 30 October 1998; accepted 16 December 1998
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1 Introduction |
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In 1986 Furchgott first suggested that endothelial-derived relaxing factor might be nitric oxide (NO) [1]. Since then the remarkable role of nitric oxide (NO) as a modulator of biological phenomena has led to the question of its involvement within the spectrum of cardiovascular disease. The resulting research has implicated NO in atherosclerosis, hypertension, cardiomyopathy, pre-eclampsia, endotoxaemia [2] and cardiac allograft rejection [3] providing important additional insights into the pathogenesis of vascular and heart muscle disease. Although initially characterised in the vasculature NO is present in heart muscle [4] whilst the relative expression of the three isoforms (ncNOS, iNOS, ecNOS) responsible for its synthesis may have important implications in disease pathology. Apart from a cytotoxic role, NO has a role in cytostasis both regulating normal homeostasis and protecting against cell injury [5]. This, has led to the hypothesis that NO is cardioprotective in ischaemic heart disease. In testing this
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2 Background |
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3 Early preconditioning |
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4 Late preconditioning |
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5 Possible mechanisms of action |
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5.1 Free radical generation
5.2 Lipopolysaccharide
5.3 Adenosine
5.4 Protein kinase C
5.5 Heat shock protein upregulation
5.6 The bradykinin–NO–cGMP hypothesis
5.7 The K ATP channel
5.8 Modulation of mitochondrial function
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6 Clinical perspective: the nitrate controversy |
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7 Future strategies |
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