dcLN and dual-lymphatic impairment impedes CSF-to-blood outflow and decreases CSF throughput. (A) Representative final frames (t = 60 min) of femoral vein showing blood content of i.c.m.-injected DB53 tracer (n = 5, 5, 6, 6; scale = 500 µm). (B) Mean traces of DB53 fluorescent intensity in blood at the femoral vein over 60 min after i.c.m. injection (mixed ANOVA: Pgroup = 0.0019, Pt = 1.4*10−10, Pgroup:t = 0.0093). (C) Comparison of area-under-curve integration of B (ANOVA: P = 0.0019, Tukey HSD: *P < 0.05, **P < 0.01). (D) Mean ICP across ligation groups (ANOVA: P = 0.70, n = 7, 7, 7, 6). (E) Mean ICP traces during constant-rate infusion (1–7 min: 0.5 μl/min, 7–13 min: 1 μl/min, 13–19 min: 2 μl/min, 19–25 min: 4 μl/min, 25–31 min: 8 μl/min). (F) Mean CSF outflow resistance across ligation conditions (ANOVA: P = 0.00091, Tukey HSD: *P < 0.05, **P < 0.01). (G) Mean CSF outflow resistance at each infusion rate (See Fig. S3 B).
Figure 4.

dcLN and dual-lymphatic impairment impedes CSF-to-blood outflow and decreases CSF throughput. (A) Representative final frames (t = 60 min) of femoral vein showing blood content of i.c.m.-injected DB53 tracer (n = 5, 5, 6, 6; scale = 500 µm). (B) Mean traces of DB53 fluorescent intensity in blood at the femoral vein over 60 min after i.c.m. injection (mixed ANOVA: Pgroup = 0.0019, Pt = 1.4*10−10, Pgroup:t = 0.0093). (C) Comparison of area-under-curve integration of B (ANOVA: P = 0.0019, Tukey HSD: *P < 0.05, **P < 0.01). (D) Mean ICP across ligation groups (ANOVA: P = 0.70, n = 7, 7, 7, 6). (E) Mean ICP traces during constant-rate infusion (1–7 min: 0.5 μl/min, 7–13 min: 1 μl/min, 13–19 min: 2 μl/min, 19–25 min: 4 μl/min, 25–31 min: 8 μl/min). (F) Mean CSF outflow resistance across ligation conditions (ANOVA: P = 0.00091, Tukey HSD: *P < 0.05, **P < 0.01). (G) Mean CSF outflow resistance at each infusion rate (See Fig. S3 B).

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