Skip to main content

Advertisement

Figure 4 | Journal of Neuroinflammation

Figure 4

From: Transient hypercapnia reveals an underlying cerebrovascular pathology in a murine model for HIV-1 associated neuroinflammation: role of NO-cGMP signaling and normalization by inhibition of cyclic nucleotide phosphodiesterase-5

Figure 4

Phosphodiesterase 5 inhibition restores vasodilatory function in Tat-transgenic mice. (A) Specificity of gisadenafil as demonstrated by measuring phosphodiesterase (PDE) activity in lysates of Cos7 cells overexpressing either PDE1A or PDE5A. (B). Maximum cerebral blood flow (CBF) reached in response to 30-second exposure to 6% CO2, as measured by laser Doppler flowmetry. The data for the untreated wild type (WT) and Tat-tg and WT mice are taken from Figure 1 (C, D); they are included here for comparison purposes. Number of animals: three for Tat-tg+BH4, five for Tat-tg + PDE5 inhibitor gisadenafil (PDEi), three for WT treated with combination of BH4 and PDEi, three for Tat-tg treated with drug combination, four for Tat-tg injected with vehicle. (C). Maximum CBF reached in response to 5-minute exposure to 6% CO2. The data for the untreated WT and Tat-tg and WT mice are taken from Figure 1 (A, B); they are included here for comparison purposes. **P <0.01, *P <0.05; n.s., not significant, nonparametric permutation test. All data represent mean ± SEM

Back to article page