|| Checking for direct PDF access through Ovid
To develop a rapid, robust, and accurate method for assessing myocardial energetics in mice and demonstrate its applicability to mouse models of acquired and genetic heart disease.We combined surface coil localization (10-mm diameter, tunable between 1H and 31P, using adiabatic half-passage radiofrequency pulses) and surgery (electrocautery removal of anterior chest wall) to create an open-chest method for acquiring in vivo 31P nuclear magnetic resonance (NMR) cardiac spectra from mice at 4.7T within 12 minutes. Normal BALB/c mice, BALB/c with myocardial infarction (MI), cardiomyocyte-restricted peroxisome proliferator-activated receptor-delta knockout (KO) (CR-PPARd–/–) and control loxP-flanked Ppard (Ppardflox/flox) mice were examined.The mean phosphocreatine (PCr)/adenosine triphosphate (ATP) ratios in control BALB/c mice, BALB/c MI mice, Ppardflox/flox mice, and PPAR-δ KO mice were 2.13 ± 0.09 (N = 11), 1.35 ± 0.07 (N = 9, P < 0.001 vs. BALB/c control), 1.92 ± 0.09 (N = 5), and 1.31 ± 0.12 (N = 5, P < 0.005 vs. Ppardflox/flox control), respectively. The significant depression of myocardial PCr/ATP we observed in these genetic/acquired models of heart disease was in accord with previous data from analogous large animal models. No NMR signal contamination from chamber blood or adjacent skeletal muscle was identified.This new technique provides cardiac 31P spectra suitable for accurate quantitative analysis in a relatively short acquisition time, is suitable for terminal studies of mouse myocardial energy metabolism, and could be installed in virtually any NMR laboratory to study myocardial energetics in numerous mouse models of human heart disease.