Purpose The aim of this study was to develop a rapid, multi-slice cardiac T1 mapping method in mice, and to apply the method to quantify manganese (Mn2+) uptake in a mouse model with altered Ca2+ channel activity. Methods An ECG-triggered multi-slice saturation-recovery Look-Locker method was developed and validated both in vitro and in vivo. A two-dose study was performed to investigate the kinetics of T1 shortening, Mn2+ relaxivity in myocardium, and the impact of Mn2+ on cardiac function. The sensitivity of Mn2+-enhanced MRI in detecting subtle changes in altered Ca2+ channel activity was evaluated in a mouse model with α-dystrobrevin knockout. Results Validation studies showed strong agreement between the current method and an established method. High Mn2+ dose led to significantly accelerated T1 shortening. Heart rate decreased during Mn2+ infusion, while ejection ratio increased slightly at the end of imaging protocol. No statistical difference in cardiac function was detected between the two dose groups. Mice with α-dystrobrevin-knockout showed enhanced Mn2+ uptake in vivo. In vitro patch-clamp study showed increased Ca2+ channel activity. Conclusion The saturation-recovery method provides rapid T1 mapping in mouse hearts, which allowed sensitive detection of subtle changes in Mn2+ uptake in α-dystrobrevin-knockout mice.

Background Altered cardiac function has been observed in cystic fibrosis transmembrane regulator (CFTR) knockout mice. However, whether this alteration is a direct effect of CFTR disruption in the heart, or is secondary due to systemic loss of CFTR, remains to be elucidated. Methods Cardiac function of mice with muscle-specific or global knockout of CFTR was evaluated at baseline and under β-stimulation by MRI in vivo. Myocyte contractility and Ca2+ transients were measured in vitro. Results Both CFTR knockout models showed increased twist and torsion at baseline. Response to β-stimulation was unaltered in muscle-specific CFTR knockout mice and was slightly decreased in global CFTR knockout mice. Aortic diameter was also decreased in both mouse models. No difference was observed in myocyte contractility and Ca2+ transients. Conclusions CFTR disruption leads to increased myocardial contractility at baseline, which may trigger untoward myocardial remodeling in CF patients that is independent of lung diseases.