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. 2017 Jun 26;2(3):258–269. doi: 10.1016/j.jacbts.2017.02.002

Figure 1.

Figure 1

Porcine Model of MI/iAL

(A) Schematic representation and image of the arterially perfused porcine wedge preparation. (B) Representative transmural optical action potentials measured from across the ventricular wall of the wedge preparation. (C) Quantification of scar size using triphenyl-tetrazolium chloride staining. (D) Images of picrosirius red (fibrosis) (top) and wheat-germ agglutinin (hypertrophy) (bottom) staining showing advanced structural remodeling in hearts from the myocardial infarction model with increased afterload (MI/iAL). (E) Bar graphs show quantitation of interstitial collagenous tissue area against the cardiomyocyte area highlighting pronounced fibrotic remodeling in MI/iAL. (F) Cx43 messenger ribonucleic acid (mRNA) expression in naive control animals (Ctrl), MI/iAL, and MI animals was not different. (G) Quantitation of fibrosis-related gene expression at the mRNA level. Connective tissue growth factor (CTGF), transforming growth factor (TGF)-β, COL1A1, and COL3A1 but not SMAD3 ere markedly up-regulated in MI/iAL hearts compared with MI and Ctrl hearts. Three pig hearts for each group were used for the reverse transcription polymerase chain reaction analyses. GAPDH = glyceraldehyde-3-phosphate dehydrogenase.