We investigated whether changes in myocardial uptake of fatty acid tracer after reperfusion following transient myocardial ischemia were closely related to alterations in intracellular fatty'/> Evaluation of Fatty Acid Metabolism in Hearts After Ischemia-Reperfusion Injury Using a Dual-Isotope Autoradiographic Approach and Tissue Assay for Metabolites of Tracer
首页> 外文期刊>The Journal of Nuclear Medicine >Evaluation of Fatty Acid Metabolism in Hearts After Ischemia-Reperfusion Injury Using a Dual-Isotope Autoradiographic Approach and Tissue Assay for Metabolites of Tracer
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Evaluation of Fatty Acid Metabolism in Hearts After Ischemia-Reperfusion Injury Using a Dual-Isotope Autoradiographic Approach and Tissue Assay for Metabolites of Tracer

机译:使用双同位素放射自显影和组织测定示踪剂代谢产物评估缺血再灌注损伤后心脏的脂肪酸代谢

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id="p-1">We investigated whether changes in myocardial uptake of fatty acid tracer after reperfusion following transient myocardial ischemia were closely related to alterations in intracellular fatty acid oxidation. >Methods: Using a fatty acid tracer of 131I- and 125I-labeled 15-(p-iodophenyl)-9-methylpentadecanoic acid (9MPA), the myocardial uptake and metabolites were determined by dual-tracer autoradiography and thin-layer chromatography in rats 3 or 14 d after reperfusion following 5 or 15 min of ischemia induced by coronary artery ligation. >Results: 9MPA metabolites processed via ?2-oxidation were lower in the ischemic region (IR) than in non-IR 3 d after 5 min of ischemia, despite no reduction of tracer uptake in IR. Oxidation of 9MPA was recovered 14 d after 15 min of ischemia in association with normalization of tracer uptake in IR, whereas both uptake and oxidation of 9MPA were markedly impaired 3 d after 15 min of ischemia, accompanied by slow clearance of myocardial tracer. >Conclusion: Normal uptake of fatty acid tracer early after reperfusion does not always imply preserved intracellular fatty acid oxidation. However, reduction of tracer uptake might reflect impaired fatty acid oxidation.
机译:id =“ p-1”>我们研究了短暂性心肌缺血后再灌注后心肌对脂肪酸示踪剂摄取的变化是否与细胞内脂肪酸氧化的改变密切相关。 >方法:使用脂肪酸示踪剂 131 I-和 125 I标记的15-( p -碘苯基)-9-甲基十五碳四烯酸(9MPA)通过双示踪放射自显影和薄层色谱法测定大鼠在冠状动脉结扎引起的缺血5或15分钟后的再灌注后3或14 d的心肌摄取和代谢产物。 >结果:缺血5分钟后,缺血区域(IR)中经α2-氧化处理的9MPA代谢物比非IR中的要低,尽管IR中的示踪剂吸收没有降低。缺血15分钟后14 d与IR示踪剂摄取正常化相关联,恢复了9MPA的氧化,而缺血15分钟后3 d显着削弱了9MPA的摄取和氧化,并伴有缓慢的心肌示踪剂清除。 >结论:再灌注后早期正常摄取脂肪酸示踪剂并不总是意味着细胞内脂肪酸氧化得以保留。但是,示踪剂摄取的减少可能反映了脂肪酸氧化受损。

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