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Effect of Postconditioning on Myocardial ^99mTc-Annexin-V Uptake: Comparison with Ischemic Preconditioning and Caspase Inhibitor Treatment

¹ Department of Biotracer Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan; ² Division of Pathology, Kanazawa Medical Center, Kanazawa, Japan; ³ Department of Laboratory Medicine, University of Washington, Seattle, Washington; ⁴ Medical and Pharmacological Research Center Foundation, Hakui, Japan; and ⁵ Division of Nuclear Medicine, Department of Radiology, Memorial Sloan-Kettering Hospital, New York, New York

Correspondence: For correspondence or reprints contact: Junichi Taki, MD, PhD, Department of Biotracer Medicine, Kanazawa University Graduate School of Medical Sciences, 13-1 Takara-machi, Kanazawa, 920-8640, Japan. E-mail: taki{at}med.kanazawa-u.ac.jp

^99mTc-Annexin-V imaging has been proved to be feasible to detect phosphatidylserine, which externalizes on the outer cell membrane early in the process of apoptosis. To determine whether postconditioning suppresses myocardial cell damage or apoptosis, we evaluated the intensity and distribution of ^99mTc-annexin-V uptake after postconditioning in a rat model of ischemia and reperfusion and compared the effect to that of ischemic preconditioning and pretreatment with caspase inhibitor. Methods: In control rats (n = 13), after thoracotomy the left coronary artery was occluded for 20 min followed by reperfusion for 30 or 90 min and injection of ^99mTc-annexin-V (80–150 MBq). One hour later, to verify the area at risk, ²⁰¹Tl (0.74 MBq) was injected intravenously just beyond the left coronary artery reocclusion, and the rats were sacrificed 1 min later. In the groups of rats with various interventions, postconditioning (n = 11) was performed just after the reperfusion, and preconditioning (n = 11) and caspase inhibitor treatment (n = 11) were performed before ischemia. Dual-tracer autoradiography was performed to assess ^99mTc-annexin-V uptake and area at risk. Results: In all control rats, intense ^99mTc-annexin-V uptake was observed in the area at risk (uptake ratios at 30 or 90 min after reperfusion, 4.15 ± 1.89 and 3.70 ± 1.41, respectively). Postconditioning suppressed ^99mTc-annexin-V uptake (uptake ratios at 30 or 90 min after reperfusion, 2.09 ± 0.56, P < 0.05, and 1.88 ± 0.69, P < 0.05, respectively). Preconditioning also suppressed uptake (uptake ratios at 30 and 90 min after reperfusion, 1.17 ± 0.29, P < 0.005, and 1.33 ± 0.74, P < 0.01, respectively), as did caspase inhibitor (uptake ratios at 30 and 90 min after reperfusion, 2.08 ± 0.50, P < 0.05, and 1.27 ± 0.24, P < 0.005, respectively). In all interventions, the percentage of cells positive on deoxyuride-5'-triphosphate biotin nick end labeling and histologic changes with myocardial cell degeneration and cell infiltrations were suppressed markedly. Conclusion: These data indicate that ^99mTc-annexin-V imaging may be a way to monitor myocardial injury and its response to novel therapeutic interventions including postconditioning, preconditioning, and antiapoptotic therapy.

Key Words: ^99mTc-annexin-V • postconditioning • ischemic preconditioning • apoptosis imaging • caspase inhibitor

COPYRIGHT © 2007 by the Society of Nuclear Medicine, Inc.

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