Abstract
This study describes the effect of superparamagnetic iron oxide on myocardial signal intensity and defines the mechanism of action of this agent. Magnetic resonance images of the heart and relaxation data were obtained in 19 rats, and another three rats were used for measurements of contrast material concentration in the heart, with the contrast agent enriched with iron-59. A dose of 36 .mu.mol of iron per kilogram induced homogeneous signal loss in the myocardium with a gated spin-echo sequence with a repetition time of 1,500 msec and an echo time of 20 msec. The reduction of signal intensity was the result of a combination of diffusion-dependent and diffusion-independent T2 shortening. The diffusion effect results from dephasing of spins moving across magnetic field gradients generated in the tissue by the contrast agent. The relative contribution of the diffusion-induced signal loss observed in vivo was larger than that predicted from the in vitro relaxation measurements. The reduced in vitro effect is likely the result of loss of a portion of the intramyocardial blood volume during sample preparation, as assessed with the Fe-59 measurements.