Quantitative T(1rho) and magnetization transfer magnetic resonance imaging of acute cerebral ischemia in the rat.

It has been previously shown that T1 in the rotating frame (T(1rho)) is a very sensitive and early marker of cerebral ischemia and that, interestingly, it can provide prognostic information about the degree of subsequent neuronal damage. In the present study the authors have quantified T(1rho) together with the rate and other variables of magnetization transfer (MT) associated with spin interactions between the bulk and semisolid macromolecular pools by means of Z spectroscopy, to examine the possible overlap of mechanisms affecting these magnetic resonance imaging contrasts. Substantial prolongation of cerebral T(1rho) was observed minutes after induction of ischemia, this change progressing in a time-dependent manner. Difference Z spectra (contralateral nonischemic minus ischemic brain tissue) showed a significant positive reminder in the time points from 0.5 to 3 hours after induction of ischemia, the polarity of this change reversing by 24 hours. Detailed analysis of the MT variables showed that the initial Z spectral changes were due to concerted increase in the maximal MT (+3%) and amount of MT (+4%). Interestingly, the MT rates derived either from the entire frequency range of Z spectra or the time constant for the first-order forward exchange (k(sat)) were unchanged at this time, these variables reducing only one day after induction of ischemia. The authors conclude that T(1rho) changes in the acute phase of ischemia coincide with both elevated maximal MT and amount of MT. These changes occur independent of the overall MT rate and in the absence of net water gain to the tissue, whereas in the consolidating infarction the decrease in the rate and amount of MT, as well as the extensive prolongation of T(1rho), are associated with water accumulation.

B0 dependence of the on-resonance longitudinal relaxation time in the rotating frame (T1rho) in protein phantoms and rat brain in vivo.

On-resonance longitudinal relaxation time in the rotating frame (T1rho) has been shown to provide unique information during the early minutes of acute stroke. In the present study, the contributions of the different relaxation mechanisms to on-resonance T1rho relaxation were assessed by determining relaxation rates (R1rho) in both protein phantoms and in rat brain at 2.35, 4.7, and 9.4 T. Similar to transverse relaxation rate (R2), R1rho increased substantially with increasing magnetic field strength (B0). The B0 dependence was more pronounced at weak spin-lock fields. In contrast to R1rho, longitudinal relaxation rate (R1) decreased as a function of increasing B0 field. The present data argue that dipole-dipole interaction forms only one pathway for T1rho relaxation and the contributions from other physicochemical factors need to be considered.

On- and off-resonance T(1rho) MRI in acute cerebral ischemia of the rat.

The ability of on-resonance T(1rho) (T(1rho)) and off-resonance T(1rho) (T(1rho)(off)) measurements to indicate acute cerebral ischemia in a rat model of transient middle cerebral artery (MCA) occlusion was investigated at 4.7 T. T(1rho) was determined with B(1) fields of 0.4, 0.8, and 1.6 G, and T(1rho)(off) with five offset frequencies ((Delta)omega) ranging from 0-7.5 kHz at B(1) of 0.4 G, yielding effective B(1) (B(eff)) from 0.4 to 1.8 G. Diffusion, T(1), and T(2) were also quantified. Both T(1rho) and T(1rho)(off) acquired with (Delta)(o)< 2.5 kHz showed positive contrast during the first hours of MCA occlusion in the ischemic tissue delineated by low diffusion. Interestingly, T(1rho)(off) contrast acquired with (Delta)omega > 2.5 kHz was clearly less sensitive to ischemic alterations, and developed with a delayed time course. This discrepancy is thought to be a consequence of the frequency dependency of cross-relaxation during irradiation with spin-lock pulses.