Influence of beta-adrenoceptor blockade on the myocardial accumulation of fatty acid tracer and its intracellular metabolism in the heart after ischemia-reperfusion injury.

Second Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama 930-0194, Japan.
Circulation Journal (Impact Factor: 3.94). 12/2006; 70(11):1509-14.
Source: PubMed


Increases in sympathetic nerve activity during ischemia may increase intracellular fatty acid (FA) accumulation via enhanced FA uptake and inhibition of beta-oxidation. Therefore, the beneficial effects of beta-adrenoceptor blockade on myocardial ischemic injury might result from the suppression of FA accumulation.
Carvedilol (1 mg/kg) or propranolol (1 mg/kg) was injected 10 min 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.
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 beta-blockade before ischemia could accelerate the recovery from ischemia-reperfusion injury by inhibiting myocardial FA accumulation before beta-oxidation.

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