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Manganese‐enhanced MRI detection of impaired calcium regulation in a mouse model of cardiac hypertrophy
Author(s) -
Andrews Martin,
Giger Maryellen L.,
Roman Brian B.
Publication year - 2015
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.3249
Subject(s) - muscle hypertrophy , medicine , creatine kinase , cardiac hypertrophy , endocrinology , calcium , chemistry , cardiology
The aim of this study was to use manganese (Mn)‐enhanced MRI (MEMRI) to detect changes in calcium handling associated with cardiac hypertrophy in a mouse model, and to determine whether the impact of creatine kinase ablation is detectable using this method. Male C57BL/6 (C57, n = 11) and male creatine kinase double‐knockout (CK‐M/Mito –/– , DBKO, n = 12) mice were imaged using the saturation recovery Look–Locker T 1 mapping sequence before and after the development of cardiac hypertrophy. Hypertrophy was induced via subcutaneous continuous 3‐day infusion of isoproterenol, and sham mice not subjected to cardiac hypertrophy were also imaged. During each scan, the contrast agent Mn was administered and the resulting change in R 1 (=1/ T 1 ) was calculated. Two anatomical regions of interest (ROIs) were considered, the left‐ventricular free wall (LVFW) and the septum, and one ROI in an Mn‐containing standard placed next to the mouse. We found statistically significant ( p < 0.05) decreases in the uptake of Mn in both the LVFW and septum following the induction of cardiac hypertrophy. No statistically significant decreases were detected in the standard, and no statistically significant differences were found among the sham mice. Using a murine model, we successfully demonstrated that changes in Mn uptake as a result of cardiac hypertrophy are detectable using the functional contrast agent and calcium mimetic Mn. Our measurements showed a decrease in the relaxivity ( R 1 ) of the myocardium following cardiac hypertrophy compared with normal control mice. Copyright © 2014 John Wiley & Sons, Ltd.