Sympathetic stimulation of ischemic myocardium: role of plasma free fatty acids and potassium.

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.