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短暂性心肌缺血后脂肪酸代谢的延迟恢复:“缺血记忆”的潜在成像靶点。

Delayed recovery of fatty acid metabolism after transient myocardial ischemia: a potential imaging target for "ischemic memory".

作者信息

Messina Steven A, Aras Omer, Dilsizian Vasken

机构信息

Division of Nuclear Medicine, Department of Diagnostic Radiology, University of Maryland Hospital and School of Medicine, Baltimore, MD 21201-1595, USA.

出版信息

Curr Cardiol Rep. 2007 Apr;9(2):159-65. doi: 10.1007/BF02938343.

Abstract

The myocardium preferentially oxidizes free fatty acids for energy production. However, the dependency of this metabolic pathway on oxygen makes this process vulnerable to ischemia. The energy requirements of the myocardium are subsequently met by the oxidation of carbohydrates, particularly glucose. Recovery of fatty acid metabolism lags behind restoration of perfusion, resulting in the phenomenon of metabolic stunning. This decrease of fatty acid utilization following ischemia can be imaged with fatty acid radiotracers, particularly beta-Methyl-p-(123)I-iodophenyl pentadecanoic acid (BMIPP), which demonstrates markedly limited metabolism via beta-oxidation, resulting in prolonged retention in the cardiomyocyte. Thus, in patients presenting with chest pain and no prior myocardial infarction, abnormal BMIPP uptake at rest reflects metabolic alteration caused by the preceding ischemia, also termed ischemic memory.

摘要

心肌优先氧化游离脂肪酸以产生能量。然而,这种代谢途径对氧气的依赖性使该过程易受缺血影响。心肌的能量需求随后通过碳水化合物(尤其是葡萄糖)的氧化来满足。脂肪酸代谢的恢复落后于灌注的恢复,导致代谢休克现象。缺血后脂肪酸利用的这种减少可用脂肪酸放射性示踪剂成像,特别是β-甲基-p-(123)I-碘苯基十五烷酸(BMIPP),它通过β-氧化显示出明显受限的代谢,导致在心肌细胞中长时间滞留。因此,在出现胸痛且无既往心肌梗死的患者中,静息时BMIPP摄取异常反映了先前缺血引起的代谢改变,也称为缺血记忆。

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