beta-
Adrenergic catecholamine discharge can be linked to local and systemic metabolic abnormalities that in turn could predispose to metabolic deterioration and
arrhythmia formation in the context of
myocardial ischemia. beta-Receptor stimulation mobilizes
free fatty acids (FFAs) and decreases blood
potassium. High
fatty acids greatly enhanced the release of
enzyme from the coronary-ligated isolated working rat heart. The combination of high circulating FFA (0.9 mM bound to
albumin 0.25 mM) and low
potassium (K+ = 3.0 mM) was particularly disadvantageous for the efficiency of myocardial contraction.
Catecholamine stimulation can be linked to serious ventricular arrhythmias in the ischemic myocardium by a combination of altered circulating metabolites and particularly by
hypokalemia. Decreasing circulating K+ from 5.9 to 3.0 mM increases the duration of
tachyarrhythmias in the isolated coronary-ligated working rat heart from 0.1 +/- 0.1 to 1.8 +/- 0.7 s/min (p less than 0.025) in
fatty acid perfused hearts and from 0.07 +/- 0.05 to 1.6 +/- 0.05 s/min (p less than 0.005) in hearts perfused with both
glucose and
fatty acid. Therefore, the systemic consequence of
catecholamine stimulation had the following effects on the ischemic myocardium (coronary artery
ligation in isolated rat heart): (a) FFAs increased
enzyme release and decreased efficiency of work ("
oxygen wastage") but were not arrhythmogenic while (b)
hypokalemia greatly enhanced
arrhythmia development and decreased mechanical efficiency of work. Further efforts should be made to study the effects of low plasma
potassium and high plasma FFA on the myocardium in patients in the early phases of acute
myocardial infarction.