Influence of β-Adrenoceptor Blockade on the Myocardial Accumulation of Fatty Acid Tracer and Its Intracellular Metabolism in the Heart After Ischemia-Reperfusion Injury

Background Increases in sympathetic nerve activity during ischemia may increase intracellular fatty acid (FA) accumulation via enhanced FA uptake and inhibition of β-oxidation. Therefore, the beneficial effects of β-adrenoceptor blockade on myocardial ischemic injury might result from the suppression of FA accumulation. Methods and Results Carvedilol (1mg/kg) or propranolol (1mg/kg) was injected 10min before 15-min occlusion of coronary artery in rats. Myocardial FA accumulation and intracellular metabolites of FA tracer were determined 3 days after reperfusion using ^<125>I- and ^<131>I-9-metylpentadecanoic acid (9MPA). Carvedilol significantly decreased 9MPA accumulation in both the ischemic region (IR) and non-IR, as compared with vehicle, and increased its clearance. However, the non-metabolized 9MPA fraction was not different between carvedilol- and vehicle-treated rats. Consequently, the amount of non-metabolized 9MPA in the myocardium was lower in rats treated with carvedilol than in those given vehicle. These effects of carvedilol were not different from those of propranolol. Conclusion Beta-adrenoceptor blockade did not affect a visual assessment of the autoradiographic image of 9MPA in hearts subjected to ischemia-reperfusion, but it accelerated the clearance of 9MPA in both the IR and non-IR. The administration of β-blockade before ischemia could accelerate the recovery from ischemia-reperfusion injury by inhibiting myocardial FA accumulation before β-oxidation.