There has been much interest in the possible physiological and pathophysiological roles of myocardial prostaglandins1. One particularly intriguing suggestion2 is that they may be capable of protecting the heart against arrhythmogenic stimuli. There is certainly no doubt that some prostaglandins can protect against a variety of arrhythmias induced either chemically or by coronary artery ligation2-4. For example, PGE2 and prostacyclin are effective against the early post-infarction arrhythmias that result from acute coronary artery ligation in anaesthetized dogs3 and rats4. In a previous study5,6 we could find no evidence that PGE2 (or PGF2α) was released from the canine myocardium at a time when ventricular ectopic activity was pronounced. We now demonstrate that, in contrast, both thromboxane and prostacyclin are released from the acutely ischaemic myocardium and that the balance between thromboxane and prostacyclin release in the period immediately following coronary artery ligation is related to the occurrence of arrhythmias.
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