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. 2019 Jun 7;14(6):e0218110. doi: 10.1371/journal.pone.0218110

Fig 3. PDE3 and PDE4 inhibition after PTX treatment increased in vivo rate of left ventricle contractility in wild type (WT) and AC5KO mice but not in AC6KO mice.

Fig 3

Left ventricular (LV) +(dP/dt)max (A-C), -(dP/dt)max (D-F) and heart rate (G-I) recorded in WT (A, D, G), AC5KO (B, E, H) and AC6KO (C, F, I) mice treated first with timolol (2.5 mg/kg i.p.) followed by combined PDE3 inhibitor cilostamide (3 mg/kg i.p.) and PDE4 inhibitor rolipram (10 mg/kg i.p.). To verify continuous and complete βAR blockade, timolol (2.5 mg/kg i.p.) was administered a second time after the PDE inhibitors. All mice received either saline or PTX injection i.p. three days prior to study. Experiments were conducted after vagotomy. Data are mean±SEM. *P<0.05, two-way repeated measures ANOVA with Tukey’s multiple comparisons test; **P<0.05, two-way ANOVA with Sidak’s multiple comparisons test; #P<0.05 PTX-treated AC6KO vs. PTX-treated WT and AC5KO, two-way ANOVA with Sidak’s multiple comparisons test. ##P<0.05 vs. baseline, Cil/Rol and the second timolol in respective saline and PTX treated groups, two-way repeated measures ANOVA with Tukey’s multiple comparisons test.