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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: Hypertension. 2018 Apr 30;71(6):1156–1163. doi: 10.1161/HYPERTENSIONAHA.118.10934

Figure 1. Minocycline attenuates monocrotaline (MCT)-induced pulmonary pathophysiology.

Figure 1

A, Right ventricular systolic pressure (RVSP) shown in controls and MCT-treated rats that were either untreated (vehicle) or treated with intracerebroventricular (ICV) minocycline. B, Measurement of right ventricular enddiastolic pressure (RVEDP). C, Ventricular contractility as shown by +dP/dt and D, -dP/dt. E, Ratio of right ventricle (RV) to left ventricle (LV) end-diastolic area (RV/LV EDA) as visualized by echocardiography and F, Ratio of RV to LV ejection fraction (EF) examined by echocardiography. ‡p<0.001 vs. control and minocycline, ***p<0.001, **p<0.01, *p<0.05 vs. MCT and †††p<0.001, ††p<0.01, †p<0.05 vs. control and minocycline (n= 6–7 rats/group); Mino = Minocycline. Data are represented as mean ± SEM, analyzed using one-way analysis of variance (ANOVA) with Newman-Keuls post hoc test. 2-way ANOVA also showed significant interactions between MCT and minocycline on RVSP (p=0.0043).