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. 2020 Sep 29;13(10):279. doi: 10.3390/ph13100279

Figure 2.

Figure 2

NG291 increases blood–brain barrier (BBB) permeability to large fluorescent dextran tracers in normal mice. (A) Image of a craniotomy over a mouse right cortex. Superficial blood vessels are clearly discernable through the glass window. (B) Maximum intensity z projection image (through the depth of 0–518 µm) from intravital confocal microscopy of a region under the cranial window in A showing the vascular network after intravenous injection of fluorescein isothiocyanate (FITC)-dextran (2 MDa). (C–J) Representative intravital confocal Z-stack images of mouse brain microvasculature (pial vessels) following i.v. injection of (C–F) tetramethylrhodamine (TRITC)-dextran (mw 155 kDa; Stoke’s radius ~ 8.5 nm) or (G–J) FITC-dextran (mw 2 MDa; Stoke’s radius ~ 27 nm) (C,E,G,I) before and 30 min post-injection of (D,H) saline or (F,J) the B2R agonist NG291 (50 µg/kg or 1.25 µg/mouse). Pseudo-color bars show fluorescence intensity scales ranging from black (no intensity) to red (high intensity). Qualitative differences in fluorescence of 155 kDa or 2 MDa dextrans between saline and NG291-treated animals are depicted (n = 3 mice/group). Dextran leakage usually occurred 60 s after NG291 injection. Injection of the vehicle did not affect BBB permeability.