Abstract #0107

In-vivo metabolism of co-hyperpolarized [1-13C] pyruvate and [1,3-13C] acetoacetate identifies cytosolic and mitochondrial redox in ischemic perfused hearts

Gaurav Sharma¹, Craig R. Malloy^1,2,3, A. Dean Sherry^1,2,4, and Chalermchai Khemtong^1,2

¹Advanced Imaging Research Center, University of Texas Southwestern Medical Center, Dallas, TX, United States, ²Department of Radiology, University of Texas Southwestern Medical Center, Dallas, TX, United States, ³Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States, ⁴Department of Chemistry, University of Texas at Dallas, Dallas, TX, United States

Cellular redox state is intricately linked with cardiac ischemia. Historically, tissue levels of lactate to pyruvate and β-hydroxybutyrate to acetoacetate have been used as indices of cytosolic and mitochondrial redox, respectively. The present study was designed to evaluate the potential of using co-hyperpolarized (HP) [1-¹³C] pyruvate and [1,3-¹³C] acetoacetate as reporters of cytosolic and mitochondrial redox, respectively. ¹³C NMR spectra of perfused rat hearts displayed increased production of both HP-lactate and HP-β-hydroxybutyrate in low flow ischemia, rotenone, and aminooxyacetate (AOA) treated hearts. The result suggests that HP-lactate and HP-β-hydroxybutyrate are sensitive metabolic markers of tissue redox in heart tissue.

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