The Monocrotaline Rat Model of Right Heart Disease Induced by Pulmonary Artery Hypertension

Figures

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  Figure 1. Evidence of right ventricular hypertrophy in MCT rats. Body weight (g) of rats following injection of 60 mg kg−1 monocrotaline (MCT; n = 10; grey) or saline (CON; n = 10; black) prior to the excision of the heart and lungs at 4 weeks post-injection (A). Wet weights of the heart and lungs normalised to the rat body weight (B). Following the dissection of the hearts, the thickness of each ventricle free wall was taken at the mid-line of the heart between the base and the apex and measurements are shown normalised to the tibial length (C). Statistical significance between CON and MCT is denoted by * p < 0.05, ** p < 0.01, **** p < 0.0001 using two-way ANOVA with multiple comparisons [49].

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  Figure 2. Evidence of RV hypertrophy 4 weeks post-injection. (A,C) show representative cardiomyocytes isolated from the RV of CON (A) and MCT (C) at 4 weeks post-injection, labelled for ryanodine receptors (RyR2, blue) and sarcolemmal marker Caveolin-3 (Cav-3, green). (E) shows the mean TTPower value that represents t-tubule regularity in CON (black) and MCT (grey) RV cardiomyocytes. Results are expressed as mean ± SEM, n = 23 RV cardiomyocytes from N = 3 CON hearts and n = 18 RV cardiomyocytes from N = 3 MCT hearts. *** p < 0.001. (B,D) show representative confocal images of fixed right ventricular (RV) tissue sections from CON (B) and MCT (D) hearts, labelled with a sarcolemma and extracellular matrix marker (wheat germ agglutinin). (F) shows the mean ± SEM cross-sectional area from N = 3 CON and N = 3 MCT hearts. MCT RV myocytes (n = 108) had a larger cross-sectional area in comparison to CON RV (n = 160) myocytes (*** p < 0.001). Modified from [51].