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. 2018 Apr 12;122(8):1084–1093. doi: 10.1161/CIRCRESAHA.117.312535

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© 2018 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 1. — Hyperpolarized lactate generation in a rodent model of cryoinfarction. A and B, Hyperpolarized MRI demonstrated intense [1-¹³C]lactate signal at both days 3 and 7 post-experimental myocardial infarction, which was normalized in rats undergoing pharmacological macrophage depletion (n=6 rats assigned per time point per group [n= 36] to give 4–6 evaluable datasets per time point per group; mean±SEM; statistical comparison by 1-way ANOVA with the Holm–Sidak correction for multiple comparisons). Higher lactate signal is detected from the anterior portion of the heart because of some inhomogeneity from the 13C surface coil; lactate signal detected from the chest wall may reflect inflammation in the healing incision. C, Flow cytometric analysis of infarct tissue confirmed predominantly inflammatory monocyte/macrophage phenotype (CD43^lohis48^hi) at day 3 and predominantly reparative (CD43^hihis48^lo/int) phenotype at day 7 and that both subsets were depleted after the administration of clodronate liposomes. *P≤0.05, **P≤0.01, ***P≤0.001. LDH indicates lactate dehydrogenase; NADH, nicotinamide adenine dinucleotide; PDH, pyruvate dehydrogenase; and TCA, tricarboxylic acid.