Hosokawa Ryohei, Nohara Ryuji, Hirai Taku, Fujibayashi Yasuhisa, Fujita Masatoshi, Kambara Naoshige, Ohba Muneo, Tadamura Eiji, Kimura Takeshi, Kita Toru
Department of Cardiovascular Medicine, and Nuclear Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Eur J Nucl Med Mol Imaging. 2005 Jan;32(1):75-83. doi: 10.1007/s00259-004-1622-x. Epub 2004 Aug 21.
123I-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (123I-BMIPP) is a fatty acid analog for single-photon emission computed tomography (SPECT) imaging that is mainly stored in the triglyceride pool. Low-dose dobutamine infusion has been reported to improve BMIPP uptake in the stunned myocardium, but the mechanism underlying this effect remains unclear. The purpose of this study was therefore to investigate the myocardial metabolism of 123I-BMIPP in the stunned myocardium under low-dose dobutamine infusion, and to elucidate the mechanism by which dobutamine improves BMIPP uptake.
Using open-chest dogs, stunned myocardium was induced by occlusion of the left anterior descending artery (LAD) for 30 min, with subsequent reperfusion (ischemia group, n=6). After direct injection of BMIPP into the LAD, myocardial extraction and retention were examined and metabolites evaluated (using high-performance liquid chromatography) during dobutamine infusion. The results in the ischemia group were compared with findings obtained in a control group under dobutamine infusion (n=6).
Dobutamine infusion significantly increased both the rapid extraction (within 30 s) of BMIPP into the myocardium (control vs ischemia group: 48+/-19% vs 66+/-14%, p<0.05) and its subsequent retention (73+/-13% vs 85+/-8%, p<0.05). The metabolites from the myocardium consisted of back diffusion of nonmetabolized BMIPP, the alpha-oxidation metabolite, intermediate metabolites, and the full-oxidation metabolite. Among these metabolites, the full-oxidation metabolite decreased significantly (from 34.0+/-20.0% to 15.8+/-9.3%, p<0.05) in the stunned regions, though back diffusion of nonmetabolized BMIPP increased (from 51.3+/-21.9% to 71.3+/-10.1%, p<0.05).
These results indicate that increased uptake of BMIPP in stunned myocardium is mainly due to decreased beta-oxidation in tissue and increased shunt retention of BMIPP in the triglyceride pool, and thereby provide further insight into the pathophysiology of stunned myocardium.
123I-（对碘苯基）-3-（R，S）-甲基十五烷酸（123I-BMIPP）是一种用于单光子发射计算机断层扫描（SPECT）成像的脂肪酸类似物，主要储存于甘油三酯池中。据报道，低剂量多巴酚丁胺输注可改善顿抑心肌对BMIPP的摄取，但其作用机制尚不清楚。因此，本研究旨在探讨低剂量多巴酚丁胺输注下顿抑心肌中123I-BMIPP的心肌代谢情况，并阐明多巴酚丁胺改善BMIPP摄取的机制。
采用开胸犬，通过阻断左前降支（LAD）30分钟，随后再灌注诱导顿抑心肌（缺血组，n = 6）。在多巴酚丁胺输注期间，将BMIPP直接注入LAD后，检测心肌摄取和滞留情况，并评估代谢产物（采用高效液相色谱法）。将缺血组的结果与多巴酚丁胺输注下对照组的结果（n = 6）进行比较。
多巴酚丁胺输注显著增加了BMIPP在心肌中的快速摄取（30秒内）（对照组与缺血组：48±19%对66±14%，p<0.05）及其随后的滞留（73±13%对85±8%，p<0.05）。心肌代谢产物包括未代谢BMIPP的反向扩散、α-氧化代谢产物、中间代谢产物和完全氧化代谢产物。在这些代谢产物中，顿抑区域的完全氧化代谢产物显著减少（从34.0±20.0%降至15.8±9.3%，p<0.05），尽管未代谢BMIPP的反向扩散增加（从51.3±21.9%增至71.3±10.1%，p<0.05）。
这些结果表明，顿抑心肌中BMIPP摄取增加主要是由于组织中β-氧化减少以及BMIPP在甘油三酯池中的分流滞留增加，从而为顿抑心肌的病理生理学提供了进一步的见解。
