Lack of dystrophin results in abnormal cerebral diffusion and perfusion in vivo.
Bottom Line: The results show that dystrophin disruption significantly decreased the mean cerebral diffusivity in both 2-month-old (7.38 ± 0.30 × 10(-4)mm(2)/s) and 10-month-old (6.93 ± 0.53 × 10(-4)mm(2)/s) mdx mice as compared to WT (8.49 ± 0.24 × 10(-4), 8.24 ± 0.25 × 10(-4)mm(2)/s, respectively).The observation of decreased perfusion in the setting of enhanced arteriogenesis may be caused by an increase of intracranial pressure from cerebral edema.This study demonstrates the defects in water handling at the BBB and consequently, abnormal perfusion associated with the absence of dystrophin.
Affiliation: Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH 44106, USA.Show MeSH
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Mentions: Using a transit time of 50 ms (Thomas, 2005), a blood T1 of 2.2 and 2.4 s at 7 T and 9.4 T, respectively (ex vivo measurement) (Dobre et al., 2007), and a tissue T1 of 1.4, 1.6, and 1.8 s, respectively, the simulated differences between the two models with CBF ranging from 100 to 400 mL/min/100 g are shown in Fig. 6. These results suggest that at a field strength of 7 T, the difference between the classic model and the Pell model was <3% when tissue T1 was 1.8 s. However, the classic model overestimated CBF by 12% to 16% when tissue T1 was 1.4 s (Figs. 6a and b). In our current study, measured tissue T1 was ~ 1.7 s. Hence, the calculated CBF difference should be within 8% compared to the Pell model. At 9.4 T, there could be an up to 12% overestimation by the classic model (Figs. 6c and d).
Affiliation: Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH 44106, USA.