In a conscious canine model, coronary occlusion leads to rapid sympathetic nervous system activation that correlates with haemodynamic deterioration and ultimate infarct size.
In order to define the temporal and quantitative relationship between the plasma concentrations of catecholamines and the extent and location of myocardial infarction, conscious dogs underwent left anterior descending or circumflex coronary occlusion with continuous haemodynamic monitoring. Plasma noradrenaline and adrenaline concentrations were measured by the serial isotope derivative method and infarction size by the creatine kinase depletion method. Rapid increases in plasma catecholamines were seen within 1 min of coronary occlusion. Within the first hour profound elevations of plasma adrenaline (10 fold) and noradrenaline (3 fold) occurred, with peak adrenaline and noradrenaline levels correlated to infarction size determined 24 h later in anterior (r =0.71; r =0.83) and posterior (r =0.89, r =0.78) infarctions. Cardiac output and mean systemic arterial blood pressure were inversely related to adrenaline (r =0.88, r =0.73) and noradrenaline (r =0.94, r =0.73) and deterioration in haemodynamics was always noted simultaneously with or preceding increases in plasma catecholamine concentrations. There were no significant differences in plasma catecholamines dependent on location of infarction. Thus, coronary occlusion in the conscious dog results in immediate haemodynamic deterioration and activation of the sympathetic nervous system, with a strong correlation between the two suggesting that activation of the sympathetic nervous system by haemodynamic reflexes may be of importance in the conscious canine model. The degree of autonomic activation within the first hour after occlusion appears to be related to the ultimate size of infarction, possibly because of the relationship between impairment of ventricular performance and infarct size.
Karlsberg et al. (Sat,) studied this question.