Abstract
123I-beta-methyl iodophenyl pentadecanoic acid (BMIPP) can visualize myocardial fatty acid metabolism and has extensive potential for diagnosing cardiac diseases such as acute coronary syndrome in the clinical setting. Increased BMIPP uptake with decreased perfusion occasionally occurs under acute reperfusion ischemia and the kinetics of BMIPP remain unclear. The present study uses the isolated rat heart model to measure kinetic changes in BMIPP under acute reperfusion ischemia. Male Wistar rats were allotted to normal control (NG), mild (MG) and severe (SG) ischemia groups. The hearts were perfused according to the Langendorff method at a constant flow rate, and BMIPP wash-in and wash-out were studied. No-flow ischemia was applied for 15 and 30 min to the MG and SG groups, followed immediately by the wash-in and wash-out study. Whole heart radioactivity was determined using an external gamma detector throughout the experiment. Rates of myocardial uptake (K1, mL/min) and clearance (k2, min(-1)) were generated using a compartmental model analysis. The same procedures and protocols were performed using (99m)Tc-sestamibi (MIBI) as a perfusion study. Perfusion pressure significantly increased and mean heart rate significantly decreased in the severe ischemia group (heart rate: 244 ± 76, 304 ± 105 and 94 ± 140 bpm; perfusion pressure: 67 ± 13, 101 ± 31 and 160 ± 84 mmHg for NG, MG and SG, respectively). MIBI-K1 significantly decreased, whereas BMIPP-K1 increased in the MG and SG groups (MIBI-K1: 3.45 ± 1.10, 1.95 ± 0.82, and 1.05 ± 0.13 mL/min; BMIPP-K (1): 3.06 ± 0.88, 3.91 ± 0.87, and 4.94 ± 1.51 mL/min for NG, MG and SG, respectively) with an inverse relationship to the severity of ischemia. MIBI-k2 increased markedly in severe ischemia (NG vs. MG: p < 0.05), whereas BMIPP-k2 did not change in the ischemic groups (MIBI-k2: 0.00072 ± 0.0011, 0.00038 ± 0.00076 and 0.043 ± 0.033; BMIPP-k2: 0.0056 ± 0.0028, 0.0029 ± 0.0010 and 0.0037 ± 0.0022 min(-1) for NG, MG and SG, respectively). Myocardial BMIPP uptake increased immediately upon reperfusion after no-flow ischemia, and was inversely related to the severity of ischemia. The increased uptake was not due to reduced clearance, but to accelerated extraction.
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