The long-lasting signal enhancement by Gd-DTPA in areas of myocardial infarction has been conventionally explained by low perfusion and an enhanced Gd distribution volume. To test whether binding of Gd to myocardial constituents is an additional factor contributing to this effect, Gd-DTPA was allowed to equilibrate between homogenized porcine myocardial tissue and physiological saline. The relaxation rate (1/T(1)) of homogenate samples (n = 61) increased in proportion (r(2) = 0.98) to the Gd concentration (0.025-0.5 mM) of the surrounding medium, with no evidence for augmented uptake. The diffusion-limited uptake was only slightly more rapid than the subsequent Gd-release. The amount of Gd released was in line with all of the Gd-DTPA in the homogenate participating in water proton relaxation. The data from this acute myocardial infarction model do not support the notion that Gd-DTPA binding in the early stages of myocardial damage contributes to delayed enhancement.
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