Division of Magnetic Resonance, Korea Basic Science Institute, Cheongwon, Chungbuk, South Korea.
NMR Biomed. 2014 Jul;27(7):835-42. doi: 10.1002/nbm.3128. Epub 2014 May 15.
In comparison to the well-documented significance of intravascular deoxyhemoglobin (deoxyHgb), the effects of dissolved oxygen on the blood-oxygen-level-dependent (BOLD) signal have not been widely reported. Based on the fact that the prolonged inspiration of high oxygen fraction gas can result in up to a sixfold increase of the baseline tissue oxygenation, the current study focused on the influence of dissolved oxygen on the BOLD signal during hyperoxia. As results, our in vitro study revealed that the r1 and r2 (relaxivities) of the oxygen-treated serum were 0.22 mM(-1) · s(-1) and 0.19 mM(-1) · s(-1) , respectively. In an in vivo experiment, hyperoxic respiration induced negative BOLD contrast (i.e. signal decrease) in 18-42% of measured brain regions, voxels with accompanying significant decreases in both the T()2 (-12.1% to -19.4%) and T1 (-5.8% to -3.3%) relaxation times. In contrast, the T()2 relaxation time significantly increased (11.2% to 14.0%) for the voxels displaying positive BOLD contrast (in 41-50% of the measured brain), which reflected a hyperoxygenation-induced reduction in tissue deoxyHgb concentration. These data imply that hyperoxia-driven BOLD signal changes are primarily determined by the counteracting effects of extravascular oxygen and intravascular deoxyHgb. Oxygen-induced magnetic susceptibility was further demonstrated by the study of 1 min hypoxia, which induced BOLD signal changes opposite to those under hyperoxia. Vasoconstriction was more common in voxels with negative BOLD contrast than in voxels with positive contrast (% change of blood volume, -9.8% to -12.8% versus 2.0% to 2.2%), which further suggests that negative BOLD contrast is mainly evoked by an increase in extravascular oxygen concentration. Conclusively, frequency shifts, which are induced by the accumulation of oxygen molecules and associated magnetic field inhomogeneity, are a significant source of the negative BOLD contrast during hyperoxia.
与血管内脱氧血红蛋白 (deoxyHgb) 的显著作用相比，溶解氧对血氧水平依赖 (BOLD) 信号的影响尚未得到广泛报道。基于长时间吸入高氧分数气体可使组织氧合增加多达六倍的事实，本研究重点关注了溶解氧在高氧状态下对 BOLD 信号的影响。结果表明，我们的体外研究显示，经过氧气处理的血清的 r1 和 r2（弛豫率）分别为 0.22 mM(-1)·s(-1)和 0.19 mM(-1)·s(-1)。在一项体内实验中，高氧呼吸引起了 18-42%测量脑区的负 BOLD 对比（即信号下降），同时伴有 T()2（-12.1%至-19.4%）和 T1（-5.8%至-3.3%）弛豫时间的显著下降。相比之下，T()2 弛豫时间显著增加（11.2%至 14.0%）的脑区显示出正 BOLD 对比（在测量脑区的 41-50%），这反映了组织脱氧 Hgb 浓度因高氧而降低。这些数据表明，高氧驱动的 BOLD 信号变化主要取决于血管外氧和血管内脱氧 Hgb 的相互拮抗作用。通过对 1 分钟缺氧的研究进一步证明了氧诱导的磁敏感性，这导致 BOLD 信号的变化与高氧状态下相反。与正 BOLD 对比脑区相比，负 BOLD 对比脑区的血管收缩更为常见（%变化的血容量，-9.8%至-12.8%比 2.0%至 2.2%），这进一步表明负 BOLD 对比主要是由血管外氧浓度的增加引起的。总之，氧分子的积累和相关磁场不均匀性引起的频率偏移是高氧状态下负 BOLD 对比的一个重要来源。
