Dynamic imaging with lanthanide chelates in normal brain: Contrast due to magnetic susceptibility effects

TLDR

The study proposes a new NMR contrast agent mechanism based on magnetic susceptibility differences. Lanthanide chelates generate magnetic‑moment–dependent susceptibility gradients that dephase spins and reduce T2‑weighted signal, with kinetics tracked at 1–8 s resolution. Injection of Gd(DTPA) and Dy(DTPA) reduces T2‑weighted brain signal by ~50 % and broadens spectral lines, with the magnitude linked to the agent’s magnetic moment and reflecting cerebral blood volume/flow rather than blood‑brain barrier disruption. © 1988 Academic Press, Inc.

Abstract

Abstract Using a one‐dimensional rapid imaging technique, we have found that injection of lanthanide chelates such as Gd(DTPA) 2− leads to a significant decrease (50%) in rat brain signal intensity at 1.45 T using T 2 ‐weighted pulse sequences; however, no effect of comparable size is observed with T 1 ‐weighted pulse sequences. The transient effect and its kinetics were followed with a temporal resolution of between 1 and 8 s. Experiments with different lanthanide chelates show that the observed decrease in signal intensity correlates with the magnetic moment of each agent but not with their longitudinal relaxivity. Three‐dimensional chemical‐shift resolved experiments demonstrate significant line broadening in brain during infusion with Dy(DTPA) 2− Our results show that the cause of this effect is the difference in susceptibility between the capillaries, containing the contrast agent, and the surrounding tissue. As a result of these susceptibility differences, field gradients are produced in the tissue and diffusion of water through these gradients leads to a loss of spin phase coherence and thus a decrease in signal intensity. We propose this as a new type of contrast agent mechanism in NMR. The effect and its kinetics are likely to be related to important physiological parameters such as cerebral blood volume and cerebral blood flow, and do not depend on a breakdown of the blood‐brain barrier as do conventional contrast agent techniques. © 1988 Academic Press, Inc.