Modification of the Thromboxane/Prostacyclin Balance as an Approach to Antiarrhythmic Therapy During Myocardial Ischaemia and Reperfusion; The Concept of Endogenous Antiarrhythmic Substances

  • James R. Parratt
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 67)

Abstract

Most of the standard approaches to antiarrhythmic therapy in myocardial ischaemia are covered elsewhere in this symposium. They include administration of drugs with various mechanisms of action that have been classified mainly on the basis of direct effects on ion chanhels. There are however, less direct, ways of reducing the severity of the different arrhythmias that arise during myocardial ischaemia and reperfusion that depend on either preventing the release (or effects at cellular level) of endogenous arrhythmogenic substances or that promote the release (or effects at cellular level) of other endogenous substances that reduce the severity of arrhythmias. A well established example of the first approach is the use of β-adrenoceptor blocking drugs to prevent the arrhythmogenic effects of adrenaline and noradrenaline released in myocardial ischaemia but there are other, less well appreciated, possibilities which are suggested by the ability of certain 5-Ht and opioid receptor antagonists to reduce ischaemic arrhythmias in experimental animals (1,2,3). Even less attention has been paid to the possibility that the myocardium might elaborate ‘endogenous antiarrhythmic substances’ during ischaemia as a protective mechanism. This concept was, I think, first enunciated by Werner Förster (4). He suggested, partly on the basis of the efficacy of various prostaglandins (and prostacyclin) in protecting against chemically-induced arrhythmias in experimental animals, that endogenous prostaglandins might have a functional role in protecting the myocardium.

Keywords

Aspirin Prostaglandin Cane Indomethacin Nifedipine 

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Copyright information

© Springer Science+Business Media Dordrecht 1987

Authors and Affiliations

  • James R. Parratt
    • 1
  1. 1.Department of Physiology & PharmacologyUniversity of StrathclydeGlasgowScotland, UK

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