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See article by Du et al. ([10], pages 919–929) in this issue. Many studies have implicated the sympathetic nervous system as being of importance in the genesis of the arrhythmias induced by myocardial ischaemia and infarction [1]. This can involve increased activity in the sympathetic system or the local release of norepinephrine from sympathetic nerve endings exposed to the extracellular conditions that occur in ischaemic tissue. Evidence to support the role of the sympathetic nervous system has included the use of drugs to modify the system or extirpation of nerves, but rarely mimics or increases sympathetic activity. It has to be remembered that, regardless of the manner in which evidence is accumulated, activation of the sympathetic system is always arrhythmogenic and that this in itself exacerbates or even triggers arrhythmias due to other causes, and will reveal any underlying tendency for arrhythmias.Despite a large number of experiments, the available evidence both supports and denies the importance of the sympathetic system. Some of the contradictions may arise from the methods or species used, or whether the pathological condition being considered is ischaemia, infarction, or reperfusion following a period of ischaemia. The latter is a distinct condition in which the mechanisms inducing arrhythmias may be very different. Furthermore, species may be an important factor. In some species (e.g. rats, rabbits, pigs), occlusion of a coronary artery results in complete ischaemia in the area downstream of the site … * Corresponding author. Tel.: +1-604-822-9531; fax: +1-604-822-9578 rsdaa{at}interchange.ubc.ca

Are the arrhythmias due to myocardial ischaemia and infarction dependent upon the sympathetic system?