Figure 1.
Biventricular conductance catheterization in a closed-chest, non-invasively ventilated mouse.
A) Hemodynamic tracings illustrating pressure volume (PV) catheters tracking from the right atrium (RA) to right ventricle (RV) via the right external jugular vein and aorta (Ao) to left ventricle (LV) via the right carotid artery via a suprasternal incision in a closed-chest mouse (*, salivary gland). B) Representative steady-state PV loops in mouse models of (i) primary and (ii) secondary right ventricular pressure overload (RVPO) (blue loops represent sham operated animals).
Figure 2.
Biventricular hemodynamics in models of primary and secondary right ventricular pressure overload (RVPO).
A) Peak systolic pressure, B) End-diastolic pressure, C) Heart rate, D) End-diastolic volume, E) End-systolic volume, F) Stroke volume, G) dP/dt max, H) Ventricular stroke work, and I) Cardiac output. *, p<0.05 vs Sham for the corresponding ventricle; †, p<0.05 vs Primary RVPO for the corresponding ventricle; ‡, p<0.05 vs the RV for the same RVPO condition.
Table 1.
Biventricular (BiV) ventriculo-arterial coupling ratios of arterial elastance (Ea) and end-systolic elastance (Ees) in the right (RV) and left ventricles (LV) using models of primary and secondary right ventricular pressure overload (RVPO).
Table 2.
Total body, lung, and right (RV) and left (LV) ventricular weights normalized to tibia length in models of primary and secondary right ventricular pressure overload (RVPO).
Figure 3.
Hypertrophic remodeling in models of primary and secondary right ventricular pressure overload (RVPO).
A) Representative histologic staining of right (RV) and left (LV) ventricular tissue and B) bar graph of RV and LV cardiomyocyte cross-sectional areas after primary and secondary RVPO. C) Western blot and D) bar graph of RV and LV calcineurin protein expression normalized to GAPDH. E) Calcineurin-Aβ (CN-PP), F) brain natriuretic peptide (BNP), G) beta-myosin heavy chain (b-MHC), and H) sarcoplasmic reticulum Ca2+ATPase (SERCa) gene expression normalized to total ribosomal RNA (rRNA). *, p<0.05 vs Sham for the corresponding ventricle; †, p<0.05 vs Primary RVPO for the corresponding ventricle; ‡, p<0.05 vs the RV for the same RVPO condition.
Figure 4.
Fibrotic remodeling in models of primary and secondary right ventricular pressure overload (RVPO).
A) Picrosirius red staining for collagen abundance and B) quantitation of percent fibrosis in the right (RV) and left ventricle (LV) after primary and secondary RVPO. C) Western blot and D) bar graph of Type I collagen normalized to GAPDH. E–F) Gene expression of transforming growth factor beta 1 (TGFβ1) and endoglin normalized to ribosomal RNA (rRNA). G–H) Quantified protein expression of phosphorylated ERK (pERK) normalized to total ERK and phosphorylated Smad-3 normalized to total Smad-3. *, p<0.05 vs Sham for the corresponding ventricle; †, p<0.05 vs Primary RVPO for the corresponding ventricle; ‡, p<0.05 vs the RV for the same RVPO condition.