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In Vivo SPECT Quantification of Transplanted Cell Survival After Engraftment Using ¹¹¹In-Tropolone in Infarcted Canine Myocardium

¹ Imaging Program, Lawson Health Research Institute, London, Ontario, Canada; ² Medical Imaging and Medical Biophysics Department, University of Western Ontario, London, Ontario, Canada; ³ Cardiac Imaging, University of Ottawa Heart Institute, Ottawa, Ontario, Canada; and ⁴ Division of Cardiology, London Health Sciences Centre, London, Ontario, Canada

Correspondence: For correspondence or reprints contact: Kimberley J. Blackwood, Lawson Health Research Institute, 268 Grosvenor St., London, ON, Canada, N6A 4V2. E-mail: kblackwo{at}lawsonimaging.ca

Current investigations of cell transplant therapies in damaged myocardium are limited by the inability to quantify cell transplant survival in vivo. We describe how the labeling of cells with ¹¹¹In can be used to monitor transplanted cell viability in a canine infarction model. Methods: We experimentally determined the contribution of the ¹¹¹In signal associated with transplanted cell (TC) death and radiolabel leakage to the measured SPECT signal when ¹¹¹In-labeled cells were transplanted into the myocardium. Three groups of experiments were performed in dogs. Radiolabel leakage was derived by labeling canine myocardium in situ with free ¹¹¹In-tropolone (n = 4). To understand the contribution of extracellular ¹¹¹In (e.g., after cell death), we developed a debris impulse response function (DIRF) by injecting lysed ¹¹¹In-labeled cells within reperfused (n = 3) and nonreperfused (n = 5) myocardial infarcts and within normal (n = 3) canine myocardium. To assess the application of the modeling derived from these experiments, ¹¹¹In-labeled cells were transplanted into infarcted myocardium (n = 4; 3.1 x 10⁷ ± 5.4 x 10⁶ cells). Serial SPECT images were acquired after direct epicardial injection to determine the time-dependent radiolabel clearance. Clearance kinetics were used to correct for ¹¹¹In associated with viable TCs. Results: ¹¹¹In clearance followed a biphasic response and was modeled as a biexponential with a short () and long () biologic half-life. The was not significantly different between experimental groups, suggesting that initial losses were due to transplantation methodology, whereas the reflected the clearance of retained ¹¹¹In. DIRF had an average of 19.4 ± 4.1 h, and the calculated from free ¹¹¹In-tropolone injected in situ was 882.7 ± 242.8 h. The measured for TCs was 74.3 h and was 71.2 h when corrections were applied. Conclusion: A new quantitative method to assess TC survival in myocardium using SPECT and ¹¹¹In has been introduced. At the limits, method accuracy is improved if appropriate corrections are applied. In vivo ¹¹¹In imaging most accurately describes cell viability half-life if is between 20 h and 37 d.

Key Words: ¹¹¹In SPECT • cell transplant survival • myocardial infarction • canine bone marrow stromal cells • cell tracking

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