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Figure 2 | Journal of Neuroinflammation

Figure 2

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 2

Acute exposure to Tat dysregulates cerebrovascular response to hypercapnic challenge. In all panels, cerebral blood flow (CBF) change in response to 30-second exposure to 6% CO2, was measured by bilateral laser Doppler flowmetry (BLDF), in c57Bl mice. (A) CBF change 48 hours after injection with saline into right hemisphere (RH). Intact left hemisphere (LH) serves as a control. Results represent mean values from three mice. (B) Maximum CBF reached in response to 6% CO2, for the data in (A). n.s.: not significant; nonparametric permutation test. (C) CBF change 48 hours after injection with Tat into RH. Intact LH serves as a control. Results represent mean values from four mice. (D) Maximum CBF reached in response to 6% CO2, for the data in (C). **P <0.01, nonparametric permutation test. (E) CBF change 48 hours after injection with heat-inactivated Tat into RH. Intact LH serves as a control. Results represent mean values from four mice. (F) Maximum CBF reached in response to 6% CO2, for the data in (E). (G) CBF change in mice 48 hours after injection with recombinant HIV-1 Env into RH. Intact LH serves as a control. Results represent mean values from four mice. (H) Maximum CBF reached in response to 6% CO2, for the data in (G). (A, C, E, F) Values are expressed as a percentage change from baseline CBF, defined as the mean CBF measured during the one- minute period immediately preceding delivery of CO2. The shadowed area along the X-axis represents the duration of the hypercapnic challenge. All data represent mean ± SEM

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