Echocardiographic evaluation of right heart failure which might be associated with DNA damage response in SU5416-hypoxia induced pulmonary hypertension rat model

Figures

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  Fig. 1. Effects of SU5416 and hypoxia on the rats’ right ventricular (RV) pressure and hypertrophy. (A) Line chart showing the changes in RVP of SuHx rats and control rats in 1- to 6-week. (B) Scatter dot plot showing the RVSP of two groups in 1-, 2-, 4- and 6-week. (C) Comparisons of the ratio of RV weight to left ventricular (LV) and interventricular septum [RV/(LV + S)]. (D) RV to BW ratio (RV/BW). (E) LV and S to BW ration [(LV + S)/BW]. Data were presented as mean ± S.E.M., control group n = 5–7, SuHx group n = 6–7, *P < 0.05, **P < 0.01, compared with control group. W: week

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  Fig. 2. Changes of pulmonary vascular medial wall thickness and RV lesions in SuHx rats. (A) Representative photomicrographs of hematoxylin and eosin (H&E) stain of pulmonary vessel cross sections, H&E stained and masson’s trichrome stain of RV sections. (B, C) Scatter dot plot showing the comparison of vessel wall thickness and vessel wall area of vessels (outside diameter > 50 μm) between the CTL and SuHx groups. (D, E) Scatter dot plot showing the comparison of cross-sectional area of right ventricle cardiomyocyte and fibrosis between two groups. Data were presented as mean ± S.E.M., control group n = 5–7, SuHx group n = 6–7, *P < 0.05, **P < 0.01, compared with the control group. W: week

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  Fig. 3. Dynamic changes in echocardiographic measurements of SuHx rats. Scatter dot plots showing the echocardiographic indexes including PAT/PET ratios (A), PAT (B), RVEDWT (C), RVESWT (D), RVEDD (E), RVESD (F), TAPSE (G), RVWTFT (H), RVDFS (I), LVEF (J), and LVFS (K) the two groups. Data were presented as mean ± S.E.M., control group n = 5–7, SuHx group n = 6–7, *P < 0.05, **P < 0.01, compared with the control group. PAT: Pulmonary acceleration time; PAT/PET: the ratio of PAT/pulmonary ejection time; RVEDWT: RV end-diastolic free-wall thickness; RVESWT: RV end-systolic free-wall thickness; RVEDD: RV end-diastolic diameter; RVESD: RV end-systolic diameter; TAPSE: Tricuspid annular plane systolic excursion; RVWTFT: RV free-wall thickness fractional thickening; RVDFS: RV diameter fractional shortening; LVEF: left ventricular ejection fraction; LVFS: left ventricular ejection fraction; W: week

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  Fig. 4. Correlation analysis of RVSP and echocardiographic measurements. RVEDWT (A), RVESWT (B), PAT/PET ratios (C) or PAT (D) measured by echocardiography in rat models of PH. Linear correlation between RVSP and RVEDWT, RVESWT, PAT/PET ratios or PAT were demonstrated

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  Fig. 5. Changes in expression level of myocardial damage and DNA damage related proteins in RV tissue of SuHx rats. (A) Representative blots for (A) SERCA2, (B) γ-H2AX, (C) p-ATM, (D) p21, (E) p-p53, p53 and GAPDH. Mean intensity for SERCA2, γ-H2AX, p-ATM, p21, (F) p-p53 and p53 blots relative to GAPDH. Data were presented as mean ± S.E.M., control group n = 5–7, SuHx group n = 6–7, *P < 0.05, **P < 0.01, compared with the control group. The gel images shown are cropped from the full-length blot images which were shown in additional file 1. W: week

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  Fig. 6. Evaluation of DNA damage in RV tissue during the process of PH in SuHx-induced rat model. (A and B) Representative images of the immunofluorescent double staining of specific smooth muscle marker α-smooth muscle actin (α-SMA, red), γ-H2AX (or p53, green) and DAPI (blue). The summary data presented the relative fluorescent intensity of γ-H2AX-positive (C) or p53-positive (D) RV cardiomyocytes, which were normalized to the control group. Data were presented as mean ± S.E.M., W: week