Myocardial Catecholamine Release in Acute Myocardial Ischaemia; Relationship to Cardiac Arrhythmias

  • R. A. Riemersma


More than 50 per cent of all deaths from acute myocardial infarction occur within the first 2 h of the onset of symptoms and often before medical help can be activated (Armstrong et al., 1972). The cause of this sudden death is generally considered to be ventricular fibrillation. There is abundant clinical evidence of enhanced sympathetic nervous activity during myocardial infarction (Gazes et al., 1959; Valori et al., 1967; Jewitt et al., 1969, Siggers et al., 1971; Webb et al., 1972; Videbaek et al., 1972; Ceremuzynski et al., 1974; Mueller and Ayres, 1978). Further, plasma catecholamine levels are raised at the earliest measurements after the onset of symptoms and have been correlated with clinical status (Strange et al., 1974; Nadeau and de Champlain, 1979) and with the occurrence of arrhythmias. In general, high plasma noradrenaline concentrations (mainly derived from sympathetic neurones) are found during acute myocardial infarction whereas raised adrenaline levels, reflexly secreted from the adrenal medulla (Ceremuzynski et al., 1969; Staszewska-Barczak, 1971) occur in patients with shock but who do not develop ventricular fibrillation (Mueller and Ayres, 1978). It is the aim of this chapter to re-examine the effects of experimental acute myocardial ischaemia on myocardial noradrenaline metabolism in relation to the development of early serious ventricular arrhythmias.


Ventricular Arrhythmia Ventricular Fibrillation Coronary Artery Occlusion Stellate Ganglion Acute Myocardial Ischaemia 
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