Comparison of the dependence of blood R₂ and R on oxygen saturation at 1.5 and 4.7 Tesla

Abstract

Gradient-echo (GRE) blood oxygen level-dependent (BOLD) effects have both intra-and extravascular contributions. To better understand the intravascular contribution in quantitative terms, the spin-echo (SE) and GRE transverse relaxation rates, R 2 and R * 2 , of isolated blood were measured as a function of oxygenation in a perfusion system. Over the normal oxygenation saturation range of blood between veins, capillaries, and arteries, the difference between these rates, R 2 ‫؍‬ R * 2 ؊ R 2 , ranged from 1.5 to 2.1 Hz at 1.5 T and from 26 to 36 Hz at 4.7 T. The blood data were used to calculate the expected intravascular BOLD effects for physiological oxygenation changes that are typical during visual activation. This modeling showed that intravascular ⌬R* 2 is caused mainly by R 2 relaxation changes, namely 85% and 78% at 1.5T and 4.7T, respectively. The simulations also show that at longer TEs (>70 ms), the intravascular contribution to the percentual BOLD change is smaller at high field than at low field, especially for GRE experiments. At shorter TE values, the opposite is the case. For pure parenchyma, the intravascular BOLD signal changes originate predominantly from venules for all TEs at low field and for short TEs at high field. At longer TEs at high field, the capillary contribution dominates. The possible influence of partial volume contributions with large vessels was also simulated, showing large (two-to threefold) increases in the total intravascular BOLD effect for both GRE and SE. Most BOLD-fMRI studies employ R* 2 contrast changes, which, compared to R 2 changes, are larger and take place both inside the vasculature and in the tissue surrounding the vessels (1,2). Hoogenraad et al. (3) recently provided an overview of these BOLD R* 2 relaxation processes and their roles in different types of experiments and brain regions. Intravascular contributions consist of intrinsic blood R* 2 relaxation, as well as additional dephasing due to susceptibility differences between blood and tissue, or changes in local blood velocity. Extravascular vessel-size-dependent effects due to vessel-tissue susceptibility differences are expected around both capillaries and larger vessels. Susceptibility-based dephasing mechanisms have been modeled (4 -6), and based on these theoretical predictions, most in vivo BOLD quantification approaches focus on extravascular R* 2 effects. However, experiments at low and intermediate field strengths have shown that the intravascular contribution of large vessels to the fMRI signal is dominant (2,7-10). When motional weighting with magnetic field gradients is employed (2,11), approximately 60 -70% of the R* 2 effect can be removed. Based on flow and diffusion considerations, such experiments remove most signals originating from inside large vessels and from arterioles and venules above 10 -20 m. The total BOLD R* 2 effect is also expected to have a substantial intravascular contribution from venules and capillaries, because R 2 effects in pure blood are very large (12)(13)(14). To b...

Caffeine alters the temporal dynamics of the visual BOLD response

“…The value of T 1B at 4 T was estimated to be 1600 ms based on published values at 1.5 and 3 T and a power law dependence of T 1B on field strength (Lu et al, 2003a,b). The M 0 + T 2 * EPI images were used as a rough estimate of M 0A exp(ÀTE/T 2B *), based on the similarity of the transverse relaxation times of arterial blood at 4.7 T and of tissue at 4 T (both around 33 ms) (Gati et al, 1997;Silvennoinen et al, 2003) and the similarity of the proton densities of blood and tissue . Before their use for normalization, the M 0 + T 2 * EPI images were smoothed with a Gaussian kernel with FWHM = 11.25 mm.…”

The interaction between magnetization transfer and blood‐oxygen‐level‐dependent effects

“…The SE relaxation rate R 2,blood,i of blood water (21,(37)(38)(39) in the individual microvascular compartments depends on the hemoglobin oxygen saturation fraction Y i or deoxygenation fraction x deoxy,i (ϭ 1 Ϫ Y i ), in which m i ϭ 0, 0.55, or 1 for the arteriolar, capillary, or venular compartments, respectively. The capillary m c (ϳ0.55) was estimated using the assumption of an exponential decay in oxygen saturation between the arterioles and venules (18).…”

Reactive hyperemia and BOLD MRI demonstrate that VEGF inhibition, age, and atherosclerosis adversely affect functional recovery in a murine model of peripheral artery disease

“…Recently, RH has been combined with BOLD MRI techniques to provide such data. The signal intensity of BOLD images is dependent on the intravascular ratio of oxy-to deoxy-hemoglobin as well as extravascular tissue-vessel susceptibility effects (21). The contribution of each component can be emphasized by the choice of pulse sequence (21).…”

“…The signal intensity of BOLD images is dependent on the intravascular ratio of oxy-to deoxy-hemoglobin as well as extravascular tissue-vessel susceptibility effects (21). The contribution of each component can be emphasized by the choice of pulse sequence (21). Several studies have confirmed the BOLD effect in muscle (22)(23)(24)(25), but have not yet utilized it to investigate pathology.…”