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Zusammenfassung:
Objectives: Delayed blood-oxygen-level-dependent (BOLD) signal oscillations reflect low blood flow and provide a non-invasive measure of perfusion in cerebrovascular diseases (1). We identified and characterized BOLD signal delay in a mouse model of stroke.
Methods: C57/BL6 mice underwent 90-minute middle cerebral artery occlusion (MCAO) (2). Anesthesia was induced with 2.5% isoflurane and adjusted to maintain normal physiological parameters (1–1.25%). Using a 7T Bruker BioSpec scanner and a cryogenically cooled RF coil, a single-slice echo planar imaging (EPI) sequence (repetition time = 0.1 s, echo time = 20 ms, flip angle = 20, voxel size 0.15 × 0.15 × 1 mm, 3400 timepoints) was acquired during MCAO. Several temporal bandpass filters were applied to assess the contribution of different physiological processes to BOLD delay (see Figure 1). Each voxel’s time series was cross-correlated with that of the venous sinus (1) to produce maps of time shift at maximum correlation (BOLD delay).
Results: A temporal delay in low frequency oscillations relative to the venous sinus was seen in ischemic tissue but not in healthy tissue. High correlations between the time courses in the ischemic tissue and venous sinus were found in the low frequency range (0.01 to 0.1 Hz), accompanied by temporal delays in the ischemic hemisphere’s BOLD signal. This was not present at higher frequency bands (see figure).
Conclusions: Temporal delays in BOLD signal in ischemic tissue are driven by low frequency oscillations and not directly by the cardiac and respiratory cycles. Variations in heart and breathing rates, which produce oscillations in the low frequency range, are the likely cause of these delays (3).
