Figure 6.

C18 Restores Cerebral Perfusion In SAH

(A) Cerebral arteries isolated from mice with SAH (2 days post-SAH induction) have reduced CFTR protein expression (n = 6), relative to arteries isolated from sham-operated controls (n = 6). C18 treatment in vivo (3 mg/kg intraperitoneally daily for 2 days) eliminated this reduction in artery CFTR protein expression (n = 6). (B) C18 treatment in vivo reduced myogenic tone in olfactory arteries isolated from mice with SAH, an effect (C) not observed in olfactory arteries isolated from CFTR KO mice. Mean maximal vessel diameters at 45 mmHg (dia_max) are sham: 113 ± 3 μm; n = 5 from 3 mice; SAH: 109 ± 6 μm; n = 6 from 6 mice; SAH+C18:104 ± 12 μm; n = 5 from 4 mice (1-way analysis of variance: p = NS); and CFTR WT: 98 ± 6 μm; n = 8 from 4 mice; CFTR KO: 110 ± 8 μm; n = 5 from 4 mice; CFTR KO+C18: 96 ± 6 μm; n = 6 from 3 mice (1-way analysis of variance: p = NS). (D) Representative magnetic resonance perfusion maps that were used to determine forebrain cortical CBF. SAH stimulated a reduction in cerebral perfusion; C18 treatment significantly improved cerebral perfusion in mice with SAH (sham: n = 10; SAH: n = 5; SAH+C18: n = 9). All data are mean ± SEM. In (A and D), *p < 0.05 for unpaired comparisons to the sham with a 1-way analysis of variance and Dunnett’s post hoc test. In (B), *p < 0.05 for unpaired comparisons to SAH with a 2-way analysis of variance and Tukey’s post hoc test. In (C), *p < 0.05 for unpaired comparisons to WT with a 2-way analysis of variance and Tukey’s post hoc test. Abbreviations as in Figures 1, 3, and 4.