Arachidonic acid breakdown occurs very soon after the onset of myocardial ischaemia with the liberation of products of the cyclooxygenase pathway. A great deal of research has clarified the role of some of these products in modulating the severity of ischaemia (and reperfusion)-induced arrhythmias and this research has recently been reviewed (Parratt 1987, 1988; Parratt et al. 1987). In summary, it appears that these products are an important biochemical determinant of arrhythmia severity. Some substances probably act as protective 'endogenous antiarrhythmic' agents; the release of others seem to intensify arrhythmia severity. It is the balance of release of these substances that appears to be important. One approach therefore to effective antiarrhythmic therapy might be to alter the balance of eicosanoid release in favour of these protective 'endogenous antiarrhythmic' agents, a concept first discussed by Werner Forster (Forster 1976). The purpose of this present short review is to summarise the available experimental evidence for such an approach. Most of this evidence is pharmacological. A more detailed discussion will be found in the articles referred to above.
|Journal||Biomedica Biochimica Acta|
|Publication status||Published - dec. 1 1988|
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