Exogenous
fatty acids may promote arrhythmias during
ischemia and reperfusion, perhaps by increasing myocardial concentrations of long-chain acylcarnitines. We therefore studied the effects of high concentrations of
fatty acids on reperfusion arrhythmias and
acylcarnitine accumulation in isolated working rat hearts subjected to regional
ischemia and reperfusion. Hearts were perfused with
buffer containing 3%
albumin, 5.9 mM K+, and either 11 mM
glucose or 11 mM
glucose plus 1.2 mM
palmitate. After 15 min of aerobic work, the left anterior descending artery was reversibly ligated for 10 min and released, and the hearts were subsequently reperfused for 3 min. Although ischemic zone
acylcarnitine accumulation after reperfusion was significantly greater in
glucose plus
palmitate-perfused hearts (247 +/- 149 vs. 717 +/- 176 nmol/g dry wt in
glucose- vs.
palmitate-perfused hearts, respectively), no significant differences in the incidence (67 vs. 44%) or duration (95 +/- 17 vs. 56 +/- 17 s) of
ventricular fibrillation (VF) were seen in
glucose or
glucose plus
palmitate hearts, respectively. Because low K+ concentration ([K+]) has been reported to increase reperfusion arrhythmias in similar models, we reduced perfusate [K+] to 4.0 mM. This significantly increased the incidence and duration of VF in hearts perfused with
glucose alone but had no effect in
palmitate-perfused hearts. We conclude that
acylcarnitine accumulation is not arrhythmogenic in this model and that
fatty acids may actually have antiarrhythmic effects if exogenous [K+] is low.